HLA-DR1 is a human leukocyte antigen (HLA) serotype that recognizes products of the DRB1*01 gene. It has been observed to be common among centenarians and is associated with several diseases including rheumatoid arthritis, penicillamine-induced myasthenia, and schizophrenia. The document provides details on the serology, haplotypes, disease associations, and genetic linkage of HLA-DR1.
Karyotypic complexity and multiclonality: Two cytogenetic parameters to be co...Georgia Bardi
Karyotypic complexity and multiclonality (either cytogenetically unrelated clones or cytogenetically related clones) represent two parameters of prognostic significance in management of patients with Myelodysplastic syndromes.
Presented by Georgia Bardi, PhD at MDS workshop in Perugia 2008. Cytogenetic data produced by Eugenia Gourgouveli and Despina Iakovaki.
The document analyzes the distribution of HLA alleles and haplotypes in Northern Portugal. It finds that the most frequent HLA-A alleles are A*02, A*01, A*03, and A*24, the most frequent HLA-B alleles are B*44 and B*35, and the most frequent HLA-C alleles are C*07 and C*04. For HLA-DRB1, the most frequent alleles are DRB1*07 and DRB1*13. The HLA-A*01-C*07-B*08-DRB1*03 and HLA-A*29-C*16-B*44-DRB1*07 haplotypes were
Cytogenetic and Molecular Characterization of Hematological Neoplasm in an Ec...Andresz26
This study characterized the cytogenetic and molecular features of hematological malignancies in an Ecuadorian population. The researchers analyzed over 4,000 patients between 1984-2012, detecting chromosome abnormalities in around 46% via conventional cytogenetics. Specific genetic fusions were also identified, including BCR-ABL (present in 95% of CML patients as the b2/a2 transcript), PML-RARA (showing the bcr2 and bcr3 transcripts but not bcr1), CBFB-MYH11 (all cases exhibited the F transcript), and MLL-AF4 (all cases displayed the e7-e8 transcript). The frequencies of some fusion gene subtypes differed from
This document discusses the FOXP3 gene as a promising candidate gene in susceptibility to generalized vitiligo. It summarizes that FOXP3 is the master transcription factor that regulates regulatory T cells, which play an important role in preventing autoimmunity. Studies have found associations between polymorphisms in the FOXP3 gene and an increased risk of vitiligo. The document argues that further investigation of FOXP3 genetic variants and their effects on regulatory T cell development and function could provide insights into vitiligo pathogenesis and potential new therapeutic approaches targeting the FOXP3 gene/regulatory T cell network.
This document summarizes a study that analyzed antigen expression patterns in different subtypes of myelodysplastic syndromes (MDS) using flow cytometry. Bone marrow samples from 30 newly diagnosed MDS patients classified as refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS), or refractory anemia with excess blasts (RAEB) were analyzed for antigen expression on granulocytic, monocytic, erythroid and lymphoid lineages. The study found no significant differences in antigen expression between subtypes for granulocytic lineages. For erythroid lineages, the percentage of CD71-positive cells was significantly lower in RAEB compared to R
This document discusses interstitial lung disease (ILD) associated with connective tissue diseases (CTDs). It begins by providing background on ILD and defining common presentations. It then discusses the classification of ILD and patterns associated with different CTDs. Common CTDs that can cause ILD are described such as systemic sclerosis, rheumatoid arthritis, and polymyositis/dermatomyositis. Risk factors, pathophysiology, epidemiology, clinical presentation, investigations including radiography and antibodies, and biomarkers for ILD associated with CTDs are summarized. Specific CT features that can help differentiate CTD-ILD from idiopathic pulmonary fibrosis are also outlined.
Karyotypic complexity and multiclonality: Two cytogenetic parameters to be co...Georgia Bardi
Karyotypic complexity and multiclonality (either cytogenetically unrelated clones or cytogenetically related clones) represent two parameters of prognostic significance in management of patients with Myelodysplastic syndromes.
Presented by Georgia Bardi, PhD at MDS workshop in Perugia 2008. Cytogenetic data produced by Eugenia Gourgouveli and Despina Iakovaki.
The document analyzes the distribution of HLA alleles and haplotypes in Northern Portugal. It finds that the most frequent HLA-A alleles are A*02, A*01, A*03, and A*24, the most frequent HLA-B alleles are B*44 and B*35, and the most frequent HLA-C alleles are C*07 and C*04. For HLA-DRB1, the most frequent alleles are DRB1*07 and DRB1*13. The HLA-A*01-C*07-B*08-DRB1*03 and HLA-A*29-C*16-B*44-DRB1*07 haplotypes were
Cytogenetic and Molecular Characterization of Hematological Neoplasm in an Ec...Andresz26
This study characterized the cytogenetic and molecular features of hematological malignancies in an Ecuadorian population. The researchers analyzed over 4,000 patients between 1984-2012, detecting chromosome abnormalities in around 46% via conventional cytogenetics. Specific genetic fusions were also identified, including BCR-ABL (present in 95% of CML patients as the b2/a2 transcript), PML-RARA (showing the bcr2 and bcr3 transcripts but not bcr1), CBFB-MYH11 (all cases exhibited the F transcript), and MLL-AF4 (all cases displayed the e7-e8 transcript). The frequencies of some fusion gene subtypes differed from
This document discusses the FOXP3 gene as a promising candidate gene in susceptibility to generalized vitiligo. It summarizes that FOXP3 is the master transcription factor that regulates regulatory T cells, which play an important role in preventing autoimmunity. Studies have found associations between polymorphisms in the FOXP3 gene and an increased risk of vitiligo. The document argues that further investigation of FOXP3 genetic variants and their effects on regulatory T cell development and function could provide insights into vitiligo pathogenesis and potential new therapeutic approaches targeting the FOXP3 gene/regulatory T cell network.
This document summarizes a study that analyzed antigen expression patterns in different subtypes of myelodysplastic syndromes (MDS) using flow cytometry. Bone marrow samples from 30 newly diagnosed MDS patients classified as refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS), or refractory anemia with excess blasts (RAEB) were analyzed for antigen expression on granulocytic, monocytic, erythroid and lymphoid lineages. The study found no significant differences in antigen expression between subtypes for granulocytic lineages. For erythroid lineages, the percentage of CD71-positive cells was significantly lower in RAEB compared to R
This document discusses interstitial lung disease (ILD) associated with connective tissue diseases (CTDs). It begins by providing background on ILD and defining common presentations. It then discusses the classification of ILD and patterns associated with different CTDs. Common CTDs that can cause ILD are described such as systemic sclerosis, rheumatoid arthritis, and polymyositis/dermatomyositis. Risk factors, pathophysiology, epidemiology, clinical presentation, investigations including radiography and antibodies, and biomarkers for ILD associated with CTDs are summarized. Specific CT features that can help differentiate CTD-ILD from idiopathic pulmonary fibrosis are also outlined.
Copy Number Variation of KIR3DL1/3DS1 in Type 1 DiabetesNikolas Pontikos
1) The study assessed the association between copy number variation of the KIR genes KIR-3DS1 and KIR-3DL1 with Type 1 Diabetes by genotyping over 800 cases and 800 controls.
2) The results showed no evidence of association between KIR-3DS1/KIR-3DL1 copy number and T1D, nor any interaction with the HLA-Bw4 ligand.
3) Future studies aim to increase sample sizes by imputing copy numbers from Immunochip data to detect potentially smaller effects that could not be detected in this study.
This document summarizes a review article on the current state and future directions of hematopoietic stem cell engineering. The review discusses how early clinical trials using first-generation gamma-retroviral vectors showed successes in treating immune deficiencies but also safety issues like leukemia. This prompted improvements in vector design, targeted gene delivery methods, and use of pluripotent stem cells. The review evaluates these new approaches and highlights the remaining challenges to developing safer and more effective hematopoietic stem cell therapies.
When Two Diseases Cross their Paths: The Diagnostic Challenge of Rheumatoid A...Crimson-Arthritis
When Two Diseases Cross their Paths: The Diagnostic Challenge of Rheumatoid Arthritis in Sickle Cell Disease Patients by Isabel M McFarlane in Researches in Arthritis & Bone Study
This document provides information about the Foundation for Sickle Cell Disease Research's (FSCDR) proposed Sickle Cell Care Network (SCCN) program. It begins with background on sickle cell disease and how its treatment infrastructure compares unfavorably to that of hemophilia. The FSCDR aims to address deficiencies in sickle cell care through the SCCN, which would establish a nationwide network of certified comprehensive treatment centers, similar to what exists for hemophilia. The document examines the need for the SCCN program by detailing current problems with sickle cell care and contrasting it with the more successful model used for hemophilia.
1) The Dlx5 homeodomain is a transcription factor linked to several human diseases. Mutations in the DLX5 gene have been associated with split hand and foot malformation syndrome 1 (SHFM1).
2) NMR spectroscopy was used to study the interaction between the Dlx5 homeodomain and DNA, identifying a 14 base pair DNA sequence (CGACTAATTAGTCG) that formed a stable complex.
3) The crystal structure of the Dlx5-DNA complex was determined at 1.85 angstrom resolution, revealing that residues associated with SHFM1 are involved in key interactions for DNA recognition and binding.
This document summarizes a study that aimed to identify subtypes of type 2 diabetes (T2D) based on clinical characteristics before diagnosis and determine if genetic risk factors differ between the subtypes. The study used clustering analysis to group 832 T2D cases into two clusters based on metabolic and anthropometric measurements. Cox proportional hazards models were then used to test if T2D genetic risk factors differed between the clusters. The clustering resulted in two clusters with cluster one having a higher percentage of women and higher values for waist-to-hip ratio, HDL, and fasting insulin. No statistically significant differences were found in genetic risk factors between the clusters, though adiposity genes were most associated with T2D risk, suggesting an interaction
This document discusses the role of HLA (human leukocyte antigen) genes in various skin diseases. It begins by describing HLA structure and function, noting that HLA genes encode antigen-presenting molecules and play a key role in the immune system. The document then examines associations between specific HLA alleles and a wide range of inflammatory, autoimmune, and infectious skin diseases. It also reviews how HLA type can influence susceptibility to drug eruptions and metabolic disorders. In conclusion, the author states that studying HLA associations with skin disease can provide insights into disease diagnosis, prognosis, clinical course, and potential new therapies.
An overview of coronaviruses. Lecture for University Biomedical Students. Using historical knowledge of coronaviruses to better understand the current SARS-CoV-2 pandemic.
The dengue virus is an arbovirus transmitted by mosquitoes that causes dengue fever and dengue hemorrhagic fever. It has four different serotypes and was first reported in Asia, Africa, and North America in 1780. The virus infects cells like phagocytes and targets tissues including the heart, liver, and brain. Symptoms of dengue hemorrhagic fever include fever, headache, vomiting blood, and plasma leakage. While there is no specific treatment, prevention efforts focus on eliminating mosquito breeding sites and repellents. Global warming and urbanization have contributed to the virus's spread to new areas, putting over 2.5 billion people at risk worldwide.
This document discusses autism spectrum disorder (ASD) and the role of comparative genomics and interactomics in furthering the understanding of ASD. It highlights that ASD is a highly heritable but genetically complex disorder, with hundreds of genes associated with it. While some genes cause syndromic forms of ASD, the majority of cases have multiple genetic variants contributing to the disorder. Comparative genomics and interactomics studies are helping to elucidate biological pathways and processes involved in ASD by analyzing genetic data from patients. This integrated genomic and systems biology approach is providing new insights into ASD pathogenesis.
This document summarizes a review article on the genetic, autoimmune, and environmental factors involved in rheumatoid arthritis (RA). It discusses how RA results from an interplay between these factors. Genetically, the HLA-DRB1 gene is a major determinant of RA risk. Over 30 non-MHC genes have also been associated with RA through genome-wide association studies and studies of specific populations, including STAT4, PADI4, and PTPN22. Environmental risks like smoking may interact with genetic susceptibility to increase RA risk. Understanding the roles of disease-associated genes and gene-environment interactions could lead to improved RA treatments and prevention strategies.
The term refractory anemia (RA) may be confusing to those who are not hematologists. RA should be well defined because it means more than what it says. RA is defined as anemia that is not responsive to therapy except transfusion.[1] The term RA is used to rule out those types of anemia with a known cause such as anemia of systemic diseases (liver and kidney) and anemia of inflammation even though they are considered refractory to therapy.[2] RA with cellular or hypercellular bone marrow was formerly used to exclude aplastic anemia.
This document discusses the morphology and classification of myelodysplastic syndromes (MDS). MDS refers to a clonal disorder of the hematopoietic stem cell that results in bone marrow failure and risk of acute leukemia. Key features include dysplasia in the peripheral blood and bone marrow seen as abnormalities in erythrocytes, granulocytes, and megakaryocytes. The diagnosis requires exclusion of other potential causes and is based on examination of blood smears, bone marrow aspirate, and biopsy showing these dysplastic features in at least two hematopoietic lineages. Classification systems such as the French-American-British system categorize MDS subtypes based on blast percentage and morphological abnormalities.
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Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Copy Number Variation of KIR3DL1/3DS1 in Type 1 DiabetesNikolas Pontikos
1) The study assessed the association between copy number variation of the KIR genes KIR-3DS1 and KIR-3DL1 with Type 1 Diabetes by genotyping over 800 cases and 800 controls.
2) The results showed no evidence of association between KIR-3DS1/KIR-3DL1 copy number and T1D, nor any interaction with the HLA-Bw4 ligand.
3) Future studies aim to increase sample sizes by imputing copy numbers from Immunochip data to detect potentially smaller effects that could not be detected in this study.
This document summarizes a review article on the current state and future directions of hematopoietic stem cell engineering. The review discusses how early clinical trials using first-generation gamma-retroviral vectors showed successes in treating immune deficiencies but also safety issues like leukemia. This prompted improvements in vector design, targeted gene delivery methods, and use of pluripotent stem cells. The review evaluates these new approaches and highlights the remaining challenges to developing safer and more effective hematopoietic stem cell therapies.
When Two Diseases Cross their Paths: The Diagnostic Challenge of Rheumatoid A...Crimson-Arthritis
When Two Diseases Cross their Paths: The Diagnostic Challenge of Rheumatoid Arthritis in Sickle Cell Disease Patients by Isabel M McFarlane in Researches in Arthritis & Bone Study
This document provides information about the Foundation for Sickle Cell Disease Research's (FSCDR) proposed Sickle Cell Care Network (SCCN) program. It begins with background on sickle cell disease and how its treatment infrastructure compares unfavorably to that of hemophilia. The FSCDR aims to address deficiencies in sickle cell care through the SCCN, which would establish a nationwide network of certified comprehensive treatment centers, similar to what exists for hemophilia. The document examines the need for the SCCN program by detailing current problems with sickle cell care and contrasting it with the more successful model used for hemophilia.
1) The Dlx5 homeodomain is a transcription factor linked to several human diseases. Mutations in the DLX5 gene have been associated with split hand and foot malformation syndrome 1 (SHFM1).
2) NMR spectroscopy was used to study the interaction between the Dlx5 homeodomain and DNA, identifying a 14 base pair DNA sequence (CGACTAATTAGTCG) that formed a stable complex.
3) The crystal structure of the Dlx5-DNA complex was determined at 1.85 angstrom resolution, revealing that residues associated with SHFM1 are involved in key interactions for DNA recognition and binding.
This document summarizes a study that aimed to identify subtypes of type 2 diabetes (T2D) based on clinical characteristics before diagnosis and determine if genetic risk factors differ between the subtypes. The study used clustering analysis to group 832 T2D cases into two clusters based on metabolic and anthropometric measurements. Cox proportional hazards models were then used to test if T2D genetic risk factors differed between the clusters. The clustering resulted in two clusters with cluster one having a higher percentage of women and higher values for waist-to-hip ratio, HDL, and fasting insulin. No statistically significant differences were found in genetic risk factors between the clusters, though adiposity genes were most associated with T2D risk, suggesting an interaction
This document discusses the role of HLA (human leukocyte antigen) genes in various skin diseases. It begins by describing HLA structure and function, noting that HLA genes encode antigen-presenting molecules and play a key role in the immune system. The document then examines associations between specific HLA alleles and a wide range of inflammatory, autoimmune, and infectious skin diseases. It also reviews how HLA type can influence susceptibility to drug eruptions and metabolic disorders. In conclusion, the author states that studying HLA associations with skin disease can provide insights into disease diagnosis, prognosis, clinical course, and potential new therapies.
An overview of coronaviruses. Lecture for University Biomedical Students. Using historical knowledge of coronaviruses to better understand the current SARS-CoV-2 pandemic.
The dengue virus is an arbovirus transmitted by mosquitoes that causes dengue fever and dengue hemorrhagic fever. It has four different serotypes and was first reported in Asia, Africa, and North America in 1780. The virus infects cells like phagocytes and targets tissues including the heart, liver, and brain. Symptoms of dengue hemorrhagic fever include fever, headache, vomiting blood, and plasma leakage. While there is no specific treatment, prevention efforts focus on eliminating mosquito breeding sites and repellents. Global warming and urbanization have contributed to the virus's spread to new areas, putting over 2.5 billion people at risk worldwide.
This document discusses autism spectrum disorder (ASD) and the role of comparative genomics and interactomics in furthering the understanding of ASD. It highlights that ASD is a highly heritable but genetically complex disorder, with hundreds of genes associated with it. While some genes cause syndromic forms of ASD, the majority of cases have multiple genetic variants contributing to the disorder. Comparative genomics and interactomics studies are helping to elucidate biological pathways and processes involved in ASD by analyzing genetic data from patients. This integrated genomic and systems biology approach is providing new insights into ASD pathogenesis.
This document summarizes a review article on the genetic, autoimmune, and environmental factors involved in rheumatoid arthritis (RA). It discusses how RA results from an interplay between these factors. Genetically, the HLA-DRB1 gene is a major determinant of RA risk. Over 30 non-MHC genes have also been associated with RA through genome-wide association studies and studies of specific populations, including STAT4, PADI4, and PTPN22. Environmental risks like smoking may interact with genetic susceptibility to increase RA risk. Understanding the roles of disease-associated genes and gene-environment interactions could lead to improved RA treatments and prevention strategies.
The term refractory anemia (RA) may be confusing to those who are not hematologists. RA should be well defined because it means more than what it says. RA is defined as anemia that is not responsive to therapy except transfusion.[1] The term RA is used to rule out those types of anemia with a known cause such as anemia of systemic diseases (liver and kidney) and anemia of inflammation even though they are considered refractory to therapy.[2] RA with cellular or hypercellular bone marrow was formerly used to exclude aplastic anemia.
This document discusses the morphology and classification of myelodysplastic syndromes (MDS). MDS refers to a clonal disorder of the hematopoietic stem cell that results in bone marrow failure and risk of acute leukemia. Key features include dysplasia in the peripheral blood and bone marrow seen as abnormalities in erythrocytes, granulocytes, and megakaryocytes. The diagnosis requires exclusion of other potential causes and is based on examination of blood smears, bone marrow aspirate, and biopsy showing these dysplastic features in at least two hematopoietic lineages. Classification systems such as the French-American-British system categorize MDS subtypes based on blast percentage and morphological abnormalities.
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Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Hla dr1 - it has been observed common centenarians
1. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 1/11
DR1 binding pocket with ligand PDB:
2G9H (https://www.rcsb.org/struct
ure/2G9H)[1]
major histocompatibility complex,
class II, DR1
Haplotypes
groups
DRA*01:DRB1*0101
DRA*01:DRB1*0102
DRA*01:DRB1*0103
Structure (See HLA-DR)
Identifiers alpha *0101
Symbol(s)
HLA-DRA (http://ww
w.gene.ucl.ac.uk/nom
enclature/data/get_da
ta.php?hgnc_id=HGN
C4947)
EBI-HLA
DRA *0101 (http://ww
w.ebi.ac.uk/cgi-bin/im
gt/hla/get_allele.cgi?
DRA*0101)
Identifiers
beta 1 *0101, *0102,
*0103 . . .
Symbol(s)
HLA-DRB1 (http://ww
w.gene.ucl.ac.uk/nom
enclature/data/get_da
ta.php?hgnc_id=495
3)
Shared data
Locus
chr.6 6p21.31 (https://
www.ncbi.nlm.nih.go
v/Omim/getmap.cgi?c
hromosome=6p21.3
1)
HLA-DR1
HLA-DR1 (DR1) is a HLA-DR serotype that recognizes the
DRB1*01 gene products. It has been observed to be common
among centenarians.[2][3][4]
Serology
Disease associations
By serotype
By allele
By genotype
By haplotype
Rheumatoid arthritis
Genetic linkage
References
The serology for the most common DR1 alleles is excellent. The
serology for alleles *0104 (https://www.ebi.ac.uk/cgi-bin/ipd/i
mgt/hla/get_allele.cgi?DRB1*0104), *0106 (https://www.ebi.ac.
uk/cgi-bin/ipd/imgt/hla/get_allele.cgi?DRB1*0106), *0109 (htt
ps://www.ebi.ac.uk/cgi-bin/ipd/imgt/hla/get_allele.cgi?DRB1*
0109), *0110 (https://www.ebi.ac.uk/cgi-bin/ipd/imgt/hla/get_
allele.cgi?DRB1*0110), *0112 (https://www.ebi.ac.uk/cgi-bin/ip
d/imgt/hla/get_allele.cgi?DRB1*0112), *0115 (https://www.ebi.
ac.uk/cgi-bin/ipd/imgt/hla/get_allele.cgi?DRB1*0115), and
*0116 (https://www.ebi.ac.uk/cgi-bin/ipd/imgt/hla/get_allele.c
gi?DRB1*0116) is unknown.
Contents
Serology
2. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 2/11
DR1 serotype recognition of Some DRB1*01 allele-group gene products[5]
DRB1* DR1 DR103 Sample
allele % % % size (N)
*0101 (https://www.ebi.ac.uk/cgi-bin/ipd/imgt/
hla/get_allele.cgi?DRB1*0101)
97% 6317
*0102 (https://www.ebi.ac.uk/cgi-bin/ipd/imgt/
hla/get_allele.cgi?DRB1*0102)
95% 2035
*0103 (https://www.ebi.ac.uk/cgi-bin/ipd/imgt/
hla/get_allele.cgi?DRB1*0103)
56% 12% 1186
*0105 (https://www.ebi.ac.uk/cgi-bin/ipd/imgt/
hla/get_allele.cgi?DRB1*0105)
>50% 2
DR1 is associated with seronegative[6]-rheumatoid arthritis,[7][8] penicillamine-induced
myasthenia,[9] and schizophrenia.[10] DR1 is increased in patients with systemic sclerosis and
arthritis[11] and in ulcerative colitis with patients that have articular manifestations.[12]
DRB1*0101 is associated with rheumatoid arthritis,[13] in anti-Jk(a) mediated hemolytic transfusion
reactions,[14] foliaceous pemphigus,[15] HTLV-1-associated myelopathy/tropical spastic paraparesis,
and [16] lichen planus.[17] In lyme disease arthritis, *0101 appears to play a role in
presentation of
triggering microbial antigens.[18]
DRB1*0102 is associated with rheumatoid arthritis,[13] in anti-Jk(a) mediated hemolytic transfusion
reactions,[14] psoriasis vulgaris,[19] and recurrent respiratory papillomatosis[20]
DRB1*0103 is associated with colonic Crohn's disease[21] and ulcerative colitis.[22][23]
DRB1*0101/*0404 and *0101/*0401 increases risk of mortality in rheumatoid arthritis, with
ischemic heart disease and smoking.[24] these same genotypes are associated with rheumatoid
vasculitis.[25]
DRB1*0102:DQB1*0501 is associated with psoriasis vulgaris[19]
and tubulointerstitial nephritis & uveitis syndrome,[26] but is
relatively protective against juvenile diabetes.[27]
DR1-DQ5 is associated with tubulointerstitial nephritis & uveitis
syndrome.[26]
Disease associations
By serotype
By allele
By genotype
By haplotype
5. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 5/11
Class Disease Associated DR 2 3 4
penicillamine-induced DR1
myositis inflammatory inclusion body DR17 DR18 DR52
narcolepsy DR2 DR12
nephritis, tubulointerstitial DR1
nephropathy IgA-mediated DR4
polyglandular deficiency syndrome DR5
pemphigus
foliaceous DR1
vulgaris DR4
psoriasis vulgaris DR1 DR7
papillomatosis, respiratory DR1
sarcoidosis non-chronic DR17 DR52
sclerosis,
multiple DR2 DR15 DR53
"bout onset" multiple DR3
systemic DR4 DR11 DR16 DR52
vulval lichen DR12
schizophrenia DR1
susceptibility
leprosy DR2
tuberculosis DR2
ragweed Ra6 allergy DR5
asthma, mite sensitive DR11
2ndary infection, AIDS DR3
aspergillosis DR15
Kaposi's sarcoma DR5
thyroid carcinomas DR8 DR11
ovarian/cervical cancer DR10 DR11 DR15
grape induced anaphylaxis DR11
Chlamydia pneumoniae DR52
thyroiditis
Hashimoto's DR3 DR5
Graves' DR3 DR17 DR52
uveitis tubulointerstitial DR1
*references are provided on linked subpages
DR1 are associated with rheumatoid arthritis, and while not the strongest association with the highest
risk for early onset arthritis is within the DR4-bearing Native American population. There frequency
of DR4-DQ8 haplotypes reach extreme nodal levels. Arthritis has been identified in a pre-Columbian
Rheumatoid arthritis
6. 10/2/22, 20:53 HLA-DR1 - Wikipedia
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DR1 Haplotypes
Serotypes DRA DRB1
DR1
*0101 *0101
*0101 *0102
*0101 *0103
Serotypes DQA1 DQB1 DRB1
DR1-DQ5 (5.1, 1)
*0101 *0501 *0101
*0101 *0501 *0102
*0101 *0501 *0103
Serotypes
HLA-
A
HLA
C
HLA
B
DRB1
A3-Cw4-B35-
DR1
*0301 *0401 *3501 *0101
A11-Cw4-B35-
DR1
*1101 *0401 *3501 *0103
A33-Cw8-B14-
DR1
*3301 *0802 *1402 *0102
remains from Italy, the affected individual bearing the DRB1*0101 allele.[28] DRB1*0101 and most
DR4 have in common a 'shared epitope'.[29][30] In this hypothesis a common region of the beta chain,
positions 67 to 74, are common and may be integral to presenting auto-immunological peptides.
HLA-DR1 is not genetically linked to DR51, DR52 or
DR53, but is linked to HLA-DQ1 and DQ5 serotypes.
1. Fernández MM, Guan R, Swaminathan CP,
Malchiodi EL, Mariuzza RA (2006). "Crystal
structure of staphylococcal enterotoxin I (SEI) in
complex with a human major histocompatibility
complex class II molecule" (https://www.ncbi.nlm.n
ih.gov/pmc/articles/PMC2730046). J. Biol. Chem.
281 (35): 25356–25364.
doi:10.1074/jbc.M603969200 (https://doi.org/10.10
74%2Fjbc.M603969200). PMC 2730046 (https://w
ww.ncbi.nlm.nih.gov/pmc/articles/PMC2730046).
PMID 16829512 (https://pubmed.ncbi.nlm.nih.gov/
16829512).
2. "The genetics of exceptional human longevity" (htt
ps://www.researchgate.net/publication/11175912).
3. Willcox, B. J.; Willcox, D. C.; He, Q.; Curb, J. D.;
Suzuki, M. (2006). "Siblings of Okinawan
Centenarians Share Lifelong Mortality
Advantages" (https://doi.org/10.1093%2Fgerona%
2F61.4.345). The Journals of Gerontology Series
A: Biological Sciences and Medical Sciences. 61
(4): 345–354. doi:10.1093/gerona/61.4.345 (http
s://doi.org/10.1093%2Fgerona%2F61.4.345).
PMID 16611700 (https://pubmed.ncbi.nlm.nih.gov/
16611700).
4. Garoyan, Georges (1990). Cent-quatorze ans de
vie ou la longue histoire de Jeanne Calment,
doyenné d'âge de France [One Hundred and
Fourteen Years of Life or the Long History of
Jeanne Calment, the Eldest of France]. Marseille:
Université d'Aix-Marseille II. pp. 22–42.
5. derived from IMGT/HLA (http://www.ebi.ac.uk/img
t/hla/allele.html)
Genetic linkage
References
7. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 7/11
6. Bardin T, Legrand L, Naveau B, Marcelli-Barge A,
Debeyre N, Lathrop G, Poirier J, Schmid M,
Ryckewaert A, Dryll A (1985). "HLA antigens and
seronegative rheumatoid arthritis" (https://www.nc
bi.nlm.nih.gov/pmc/articles/PMC1001567). Ann
Rheum Dis. 44 (1): 50–53.
doi:10.1136/ard.44.1.50 (https://doi.org/10.1136%
2Fard.44.1.50). PMC 1001567 (https://www.ncbi.n
lm.nih.gov/pmc/articles/PMC1001567).
PMID 3855618 (https://pubmed.ncbi.nlm.nih.gov/3
855618).
7. Schiff B, Mizrachi Y, Orgad S, Yaron M, Gazit E
(1982). "Association of HLA-Aw31 and HLA-DR1
with adult rheumatoid arthritis" (https://www.ncbi.nl
m.nih.gov/pmc/articles/PMC1000958). Ann
Rheum Dis. 41 (4): 403–404.
doi:10.1136/ard.41.4.403 (https://doi.org/10.113
6%2Fard.41.4.403). PMC 1000958 (https://www.n
cbi.nlm.nih.gov/pmc/articles/PMC1000958).
PMID 6981387 (https://pubmed.ncbi.nlm.nih.gov/6
981387).
8. "HLA-DR antigens in rheumatoid arthritis. A Swiss
collaborative study; final report. Swiss Federal
Commission for the Rheumatic Diseases,
Subcommission for Research". Rheumatol Int. 6
(2): 89–92. 1986. doi:10.1007/bf00541511 (https://
doi.org/10.1007%2Fbf00541511). PMID 3489975
(https://pubmed.ncbi.nlm.nih.gov/3489975).
S2CID 189901283 (https://api.semanticscholar.or
g/CorpusID:189901283).
9. Delamere J, Jobson S, Mackintosh L, Wells L,
Walton K (1983). "Penicillamine-induced
myasthenia in rheumatoid arthritis: its clinical and
genetic features" (https://www.ncbi.nlm.nih.gov/pm
c/articles/PMC1001283). Ann Rheum Dis. 42 (5):
500–504. doi:10.1136/ard.42.5.500 (https://doi.or
g/10.1136%2Fard.42.5.500). PMC 1001283 (http
s://www.ncbi.nlm.nih.gov/pmc/articles/PMC100128
3). PMID 6605118 (https://pubmed.ncbi.nlm.nih.go
v/6605118).
10. Narita K, Sasaki T, Akaho R, Okazaki Y, Kusumi I,
Kato T, Hashimoto O, Fukuda R, Koyama T,
Matsuo K, Okabe Y, Nanko S, Hohjoh H,
Tokunaga K (2000). "Human leukocyte antigen
and season of birth in Japanese patients with
schizophrenia". Am J Psychiatry. 157 (7): 1173–
1175. doi:10.1176/appi.ajp.157.7.1173 (https://doi.
org/10.1176%2Fappi.ajp.157.7.1173).
PMID 10873932 (https://pubmed.ncbi.nlm.nih.gov/
10873932).
8. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 8/11
11. Szücs G, Szekanecz Z, Zilahi E, et al. (2007).
"Systemic sclerosis-rheumatoid arthritis overlap
syndrome: a unique combination of features
suggests a distinct genetic, serological and clinical
entity" (https://doi.org/10.1093%2Frheumatology%
2Fkem021). Rheumatology (Oxford, England). 46
(6): 989–993. doi:10.1093/rheumatology/kem021
(https://doi.org/10.1093%2Frheumatology%2Fkem
021). PMID 17384178 (https://pubmed.ncbi.nlm.ni
h.gov/17384178).
12. Núñez C, Alecsandru DM, Mendoza JL, et al.
(2006). "Genetic markers linked to rheumatoid
arthritis are also strongly associated with articular
manifestations in ulcerative colitis patients". Hum.
Immunol. 67 (4–5): 324–330.
doi:10.1016/j.humimm.2006.02.035 (https://doi.or
g/10.1016%2Fj.humimm.2006.02.035).
PMID 16720213 (https://pubmed.ncbi.nlm.nih.gov/
16720213).
13. Kapitány A, Zilahi E, Szántó S, et al. (2005).
"Association of rheumatoid arthritis with HLA-DR1
and HLA-DR4 in Hungary". Ann. N. Y. Acad. Sci.
1051 (1): 263–270.
Bibcode:2005NYASA1051..263K (https://ui.adsab
s.harvard.edu/abs/2005NYASA1051..263K).
doi:10.1196/annals.1361.067 (https://doi.org/10.11
96%2Fannals.1361.067). PMID 16126967 (https://
pubmed.ncbi.nlm.nih.gov/16126967).
S2CID 6515443 (https://api.semanticscholar.org/C
orpusID:6515443).
14. Reviron D, Dettori I, Ferrera V, et al. (2005). "HLA-
DRB1 alleles and Jk(a) immunization".
Transfusion. 45 (6): 956–959. doi:10.1111/j.1537-
2995.2005.04366.x (https://doi.org/10.1111%2Fj.1
537-2995.2005.04366.x). PMID 15934994 (https://
pubmed.ncbi.nlm.nih.gov/15934994).
S2CID 20473677 (https://api.semanticscholar.org/
CorpusID:20473677).
15. del Mar Sáez-de-Ocariz M, Vega-Memije M,
Zúñiga J, Salgado N, Ruíz J, Balbuena A,
Domínguez-Soto L, Granados J (2005). "HLA-
DRB1*0101 is associated with foliaceous
pemphigus in Mexicans". Int J Dermatol. 44 (4):
350. doi:10.1111/j.1365-4632.2005.02038.x (http
s://doi.org/10.1111%2Fj.1365-4632.2005.02038.x).
PMID 15811100 (https://pubmed.ncbi.nlm.nih.gov/
15811100). S2CID 21880556 (https://api.semantic
scholar.org/CorpusID:21880556).
9. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 9/11
16. Sabouri A, Saito M, Usuku K, Bajestan S,
Mahmoudi M, Forughipour M, Sabouri Z,
Abbaspour Z, Goharjoo M, Khayami E, Hasani A,
Izumo S, Arimura K, Farid R, Osame M (2005).
"Differences in viral and host genetic risk factors
for development of human T-cell lymphotropic
virus type 1 (HTLV-1)-associated
myelopathy/tropical spastic paraparesis between
Iranian and Japanese HTLV-1-infected individuals"
(https://doi.org/10.1099%2Fvir.0.80509-0). J Gen
Virol. 86 (Pt 3): 773–781. doi:10.1099/vir.0.80509-
0 (https://doi.org/10.1099%2Fvir.0.80509-0).
PMID 15722539 (https://pubmed.ncbi.nlm.nih.gov/
15722539).
17. Luis-Montoya P, Yamamoto-Furusho JK, Vega-
Memije E, et al. (2007). "HLA-DRB1*0101 is
associated with the genetic susceptibility to
develop lichen planus in the Mexican Mestizo
population". Archives of Dermatological Research.
299 (8): 405–407. doi:10.1007/s00403-007-0769-
2 (https://doi.org/10.1007%2Fs00403-007-0769-
2). PMID 17665209 (https://pubmed.ncbi.nlm.nih.g
ov/17665209). S2CID 5986703 (https://api.semant
icscholar.org/CorpusID:5986703).
18. Steere AC, Klitz W, Drouin EE, et al. (2006).
"Antibiotic-refractory Lyme arthritis is associated
with HLA-DR molecules that bind a Borrelia
burgdorferi peptide" (https://www.ncbi.nlm.nih.gov/
pmc/articles/PMC3212725). J. Exp. Med. 203 (4):
961–971. doi:10.1084/jem.20052471 (https://doi.o
rg/10.1084%2Fjem.20052471). PMC 3212725 (htt
ps://www.ncbi.nlm.nih.gov/pmc/articles/PMC32127
25). PMID 16585267 (https://pubmed.ncbi.nlm.nih.
gov/16585267).
19. Cardoso C, Uthida-Tanaka A, Magalhães R,
Magna L, Kraemer M (2005). "Association
between psoriasis vulgaris and MHC-DRB, -DQB
genes as a contribution to disease diagnosis". Eur
J Dermatol. 15 (3): 159–63. PMID 15908298 (http
s://pubmed.ncbi.nlm.nih.gov/15908298).
20. Bonagura V, Vambutas A, DeVoti J, Rosenthal D,
Steinberg B, Abramson A, Shikowitz M, Gjertson
D, Reed E (2004). "HLA alleles, IFN-gamma
responses to HPV-11 E6, and disease severity in
patients with recurrent respiratory papillomatosis".
Hum Immunol. 65 (8): 773–782.
doi:10.1016/j.humimm.2004.05.014 (https://doi.or
g/10.1016%2Fj.humimm.2004.05.014).
PMID 15336778 (https://pubmed.ncbi.nlm.nih.gov/
15336778).
10. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 10/11
21. Fernandez L, Mendoza J, Martinez A, Urcelay E,
Fernandez-Arquero M, Garcia-Paredes J, Peña A,
Diaz-Rubio M, de la Concha E (2004). "IBD1 and
IBD3 determine location of Crohn's disease in the
Spanish population". Inflamm Bowel Dis. 10 (6):
715–722. doi:10.1097/00054725-200411000-
00004 (https://doi.org/10.1097%2F00054725-200
411000-00004). PMID 15626888 (https://pubmed.
ncbi.nlm.nih.gov/15626888). S2CID 23790673 (htt
ps://api.semanticscholar.org/CorpusID:23790673).
22. Puzanowska B, Prokopowicz D, Ziarko S,
Radziwon P, Lapinski T (2003). "The incidence of
HLA DRB1*0103 in ulcerative colitis patients in
north-eastern Poland". Hepatogastroenterology.
50 (53): 1436–8. PMID 14571756 (https://pubmed.
ncbi.nlm.nih.gov/14571756).
23. Roussomoustakaki M, Satsangi J, Welsh K, Louis
E, Fanning G, Targan S, Landers C, Jewell D
(1997). "Genetic markers may predict disease
behavior in patients with ulcerative colitis".
Gastroenterology. 112 (6): 1845–1853.
doi:10.1053/gast.1997.v112.pm9178675 (https://d
oi.org/10.1053%2Fgast.1997.v112.pm9178675).
PMID 9178675 (https://pubmed.ncbi.nlm.nih.gov/9
178675).
24. Mattey DL, Thomson W, Ollier WE, et al. (2007).
"Association of DRB1 shared epitope genotypes
with early mortality in rheumatoid arthritis: results
of eighteen years of followup from the early
rheumatoid arthritis study". Arthritis Rheum. 56
(5): 1408–1416. doi:10.1002/art.22527 (https://doi.
org/10.1002%2Fart.22527). PMID 17469097 (http
s://pubmed.ncbi.nlm.nih.gov/17469097).
25. Gorman JD, David-Vaudey E, Pai M, Lum RF,
Criswell LA (2004). "Particular HLA-DRB1 shared
epitope genotypes are strongly associated with
rheumatoid vasculitis". Arthritis Rheum. 50 (11):
3476–3484. doi:10.1002/art.20588 (https://doi.org/
10.1002%2Fart.20588). PMID 15529352 (https://p
ubmed.ncbi.nlm.nih.gov/15529352).
26. Levinson R, Park M, Rikkers S, Reed E, Smith J,
Martin T, Rosenbaum J, Foster C, Sherman M,
Holland G (2003). "Strong associations between
specific HLA-DQ and HLA-DR alleles and the
tubulointerstitial nephritis and uveitis syndrome" (h
ttps://doi.org/10.1167%2Fiovs.02-0376). Invest
Ophthalmol Vis Sci. 44 (2): 653–657.
doi:10.1167/iovs.02-0376 (https://doi.org/10.116
7%2Fiovs.02-0376). PMID 12556395 (https://pub
med.ncbi.nlm.nih.gov/12556395).
11. 10/2/22, 20:53 HLA-DR1 - Wikipedia
https://en.wikipedia.org/wiki/HLA-DR1 11/11
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27. Thomson G, Valdes AM, Noble JA, et al. (2007).
"Relative predispositional effects of HLA class II
DRB1-DQB1 haplotypes and genotypes on type 1
diabetes: a meta-analysis". Tissue Antigens. 70
(2): 110–127. doi:10.1111/j.1399-
0039.2007.00867.x (https://doi.org/10.1111%2Fj.1
399-0039.2007.00867.x). PMID 17610416 (https://
pubmed.ncbi.nlm.nih.gov/17610416).
28. Fontecchio G, Fioroni MA, Azzarone R, et al.
(2007). "Genetic predisposition to rheumatoid
arthritis in a Tuscan (Italy) ancient human remain".
International Journal of Immunopathology and
Pharmacology. 20 (1): 103–9.
doi:10.1177/039463200702000112 (https://doi.org/
10.1177%2F039463200702000112).
PMID 17346433 (https://pubmed.ncbi.nlm.nih.gov/
17346433). S2CID 2067413 (https://api.semantics
cholar.org/CorpusID:2067413).
29. Gregersen PK, Silver J, Winchester RJ (1987).
"The shared epitope hypothesis. An approach to
understanding the molecular genetics of
susceptibility to rheumatoid arthritis" (https://doi.or
g/10.1002%2Fart.1780301102). Arthritis Rheum.
30 (11): 1205–1213. doi:10.1002/art.1780301102
(https://doi.org/10.1002%2Fart.1780301102).
PMID 2446635 (https://pubmed.ncbi.nlm.nih.gov/2
446635).
30. Morel PA, Erlich HA, Fathman CG (1988). "A new
look at the shared epitope hypothesis". Am. J.
Med. 85 (6A): 20–22. doi:10.1016/0002-
9343(88)90375-0 (https://doi.org/10.1016%2F000
2-9343%2888%2990375-0). PMID 2462347 (http
s://pubmed.ncbi.nlm.nih.gov/2462347).