dendritic cells are part of innate immune system, antigen presenting cells in skin, activation of t cells and inducing and maintaining immune tolerance, 4 types- langerhans cells, dermal dendritic cells, merkel cells, melanocytes
Merkel cells (MCs) constitute a very unique population of postmitotic cells scattered along the dermoepidermal
junction. These cells that have synaptic contacts with somatosensory afferents are regarded
to have a pivotal role in sensory discernment. Several concerns exist till date as to their origin,
multiplication, and relevance in skin biology.
Pigmentation disorders of skin dermatology revision notesTONY SCARIA
dermatology revision notes for neet pg preparation based on lecture notes with high yield topic & last minute revision notes based on previous year questions
This presentation includes -classification, biological in psoriasis,TNF alpha inbitors, T cell inhibitos, IL-12/23 inhibitors (indications,containdications,guidelines, adverse effects)
dendritic cells are part of innate immune system, antigen presenting cells in skin, activation of t cells and inducing and maintaining immune tolerance, 4 types- langerhans cells, dermal dendritic cells, merkel cells, melanocytes
Merkel cells (MCs) constitute a very unique population of postmitotic cells scattered along the dermoepidermal
junction. These cells that have synaptic contacts with somatosensory afferents are regarded
to have a pivotal role in sensory discernment. Several concerns exist till date as to their origin,
multiplication, and relevance in skin biology.
Pigmentation disorders of skin dermatology revision notesTONY SCARIA
dermatology revision notes for neet pg preparation based on lecture notes with high yield topic & last minute revision notes based on previous year questions
This presentation includes -classification, biological in psoriasis,TNF alpha inbitors, T cell inhibitos, IL-12/23 inhibitors (indications,containdications,guidelines, adverse effects)
By DR. MANPREET KAUR BEHL.
Description of classificaton of immune system, immune cells, HLA, MHC complexes, antigen presentation, t-cell responses and b-cell responses, antibody, isotype switching, hypersenstivity reactions etc.
Describes the basic properties and mechanisms of T cells and B cells in maintaining Immune Response against foreign antigens or infections and covers the UG and PG portion of immunology.
A brief covering basics of immunity understanding and also allowing students to understand with ease the concepts of innate immunity, adaptive immunity, Tcell, Bcell, MHC molecular genetics, and also cytokines and also its role in various disease.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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2. Invading
microbes
(pathogens)
External defenses -1ST Line
Skin
Mucous membranes
Secretions
INNATE IMMUNITY
Rapid responses to a
broad range of microbes
ADAPTIVE IMMUNITY
Slower responses to
specific microbes
Internal defenses - 2nd Line
Phagocytic cells
Inflammatory response
Humoral response
(antibodies)Antimicrobial peptides
Natural killer cells Cell-mediated response
(cytotoxic
lymphocytes)
3.
4.
The innate immune system effectively prevent free
growth of bacteria within the body.
however, many pathogens have evolved mechanisms
allowing them to bypass the innate immune system and
generates a threshold level of antigen which triggers the
adaptive immune system .
Adaptive immunity
5.
1. The RECOGNITION of specific “non-self” antigens in the
presence of “self”, during the process of ANTIGEN
PRESENTATION.
2. The generation of TAILORED RESPONSES to eliminate
specific pathogens.
3. The development of IMMUNOLOGIC MEMORY in which
each pathogen is “remembered” by a signature antibody.
These memory cells can be called upon to quickly eliminate
a pathogen on subsequent infections due to enhancement
with each successive antigen encounter owing to the
accumulation of “memory” .
Functions of the adaptive
immune system
6.
The lymphocytes of the adaptive immune system
are:
• T cells mature in the thymus
• B cells mature in the bone marrow
The process starts by antigen presentation.
Adaptive immune system
7.
It has two separate but overlapping arms:
I. Humoral, or antibody-mediated (B Cell)
immunity
II. Cellular, or cell-mediated (T Cell) immunity
Adaptive immune
system
8.
9.
10.
1. Foreign substances
Mainly proteins, often microorganisms and their toxins
2. Human cells that have been transformed
May be tumor cells, or cells infected with viruses
3. Human tissue
Organ transplants, tissue grafts, incompatible blood
types during a transfusion
4. Autoimmune diseases
Tissue from the person’s own body becomes an
antigen
Antigens
11.
With the exception of non-nucleated cells all cells are capable
of presenting antigen and of activating the adaptive
response.
- depending on how and where the antigen first encounters
cells of the immune system.
- Some cells are specially equipped to present antigen, and
to prime naive T cells and are termed professional (APC).
Dendritic cells: Langerhans cells (LCs) are key APCs.
B-cells
Macrophages
Neutrophils
Antigen presenting
cells (APCs)
12.
Defined as professional APCs that display an
extraordinary capacity to stimulate naive T cells and
initiate a primary immune response.
Dendritic cells (DC)
13. Dendritic Cells of the epidermis.
Derived from the bone marrow
EXPRESSES:
1. Birbeck granules
2. Langerin
3. MHC class II.
4. CD1, useful marker for LCs, since within the epidermis
(normal or inflamed) it is exclusively expressed on LCs.
5. S100 ptn
6. Vimentin
7. FcεRI
Derived from the bone marrow from CD34 precursor cells.
LNGERHANS CELLS
14.
LCs cannot be identified in routinely fixed and stained
histologic sections; their recognition requires electron
microscopy or histochemical analysis.
Numbers of LCs are reduced in following:
1. The palms and soles, genitalia and buccal mucosa.
2. With age.
3. Chronically UV-exposed skin.
LNGERHANS CELLS
15.
16.
Langerhans cells can be visualized by staining using an
antibody against MHC class II molecules. Note the
dendritic shape of Langerhans cells.
17. Electron microscopic picture of a Langerhans cell. Arrows
indicate The Birbeck granules, rod-shaped organelles
specific for Langerhans cells. They are said to resemble
tennis rackets
18.
Resident Langerhans cell engulfs the exogenous
antigen or express the endogenous one
Starts emigration to the lymph nodes to meet the T
cells.
During this trip it develops some changes to become
similar to mature Dendritic cell.
LC: Antigen presentation
19.
:
a) Molecules involved in antigen uptake as Birbeck
granules, Fc receptors
b) Molecules mediating the attachment to neighboring
keratinocytes ( E-Cadherins).
:
a) Expression of receptors involved in tissue homing at
the lymph nodes as CD44.
b) Surface molecules necessary for antigen presentation
and T cell priming as MHC class I, MHC class II,
CD40, CD54, CD58, CD80, CD86.
c) Type IV collagenase enable their penetration through
the basement membrane.
d) Their dendricity becomes more pronounced.
Changes of LCs during
migration
20.
APC to B cells and T cells is not the same.
T cells only identify the antigen when processed into
peptides bound to specific surface molecules on
APC.
B cells can identify the whole antigen by antibodies
on their surface
Ag Presentation to
T-Cells
21.
T-cells identify the processed antigen bound to MHC
on the surface of Dendritic cells.
T helper CD4 T cells identify antigens bound to
MHC II while;
Cytotoxic CD8 T cells identify antigen T cells bound
to MHC I
Exogenous and endogenous antigen presentation.
Ag Presentation to
T-Cells
23.
The MHC complex is divided into three subgroups
called MHC class I, MHC class II and MHC class III.
MHC class I is present on all nucleated cells (except
RBCs).
MHC class II is present on antigen presenting cells.
MHC
25.
1. Exogenous antigens:
are engulfed by the APC, processed and presented in
association with MHC II.
2. Endogenous antigens:
(VIRUS AND TUMOURS) are processed and presented
in association with MHC I
TYPES OF AP to T-
cells
26.
27. lymphocytes
T cells undergo thymic education through positive and negative selection.
They are taught the difference between self and non-self molecules in
their school to achieve Immunologic tolerance.
28. T cells develop and mature in the Thymus after migration of the
stem cells from the bone marrow.
At the thymus only T cells that can recognize foreign and
not self antigen in the MHC complex get a survival signal
(positive selection) and pass to the circulation and lymph
nodes.
Those who fail have affinity to self antigens receive
signals for apoptosis (negative selection) thus no auto
attack.
Positive and negative selection allow the survival of just those T
cells that recognize foreign (but not “self”) peptides in the context
of “self” MHC molecules and thus are useful for immune defense
without causing auto-attack
T cells
29.
1. Immature T cells:
Express both CD4 and CD8 molecules.
2. Mature T cells:
Later with the development of the T-cell receptor
(TCR), they either express:
a)CD4 and become T helper cell that binds
antigens in MHCII
b)CD8 molecule and becomes T cytotoxic cell that
binds antigens on MHCI.
Types of T cells
30.
It is the part responsible for recognition of the specific
antigen and the further T cell response.
TCR are transmembrane molecules that are mainly of
the α/β type while only 10% are of the γ/δ type in body
and skin.
The T-CELL
RECEPTOR (TCR)
31.
Do not follow the classic way of antigen recognition .
May play a role in innate immunity.
Increase in the skin in leprosy and lieshmaniasis.
γ/δ T-cells
32.
Can recognize a huge number of antigens encoded
by more than 400 genes that are modified and
rearranged to cover an endless number of antigens
by recombination activation genes
when defective ----combined immune deficiency.
TCR
33.
CD3 is an important part of TCR responsible
for transmission of the signal to the cell that
encodes for the cytokine needed to stimulate
the required response for that particular
antigen.
TCR SIGNALLING
34.
35. Signaling through the TCR complex alone does not
suffice to activate T cells. The presence of costimulatory
signals is needed for T cells to undergo antigen-specific
clonal expansion.
Development of a productive T-cell immune response
requires exposure of these cells to at least two types of
stimuli.
The first signal is the interaction of the TCR with
peptide–MHC complexes presented by APCs, which
determines the specificity of the immune response.
The second signal involves surface molecules and
cytokines, which determine the clonal expansion of
specific T cells and their differentiation into effector
and memory cells.
Costimulatory molecules
36.
B7 FAMILY e.g. B7-1 (CD80) and B7-2 (CD86)
induced by cytokines (TNF, IL-1) or by various TLR
ligands
Cytokines, especially inflammatory mediators
like IL-1, IL-6 and TNF-α, also provide
costimulatory signals by themselves and, in
addition, upregulate costimulatory molecules.
Are very important for completion of the T-cell
response other wise ANERGY (non-reactivity)
and failure of T-cell stimulation occurs.
Costimulatory molecules
37.
38.
After proper antigen presentation
and costimulation T cell
becomes activated division
occurs.
Memory T cells develop
CLONAL EXPANSION
39.
Majority are:
In the dermis.
CD4 OR CD8.
α/β TCR.
memory phenotype CD45RO+/CD45RA-
Skin homing receptor CLA(cutaneous
lymphocyte associated antigen).
Criteria of Skin T cells
40.
1. CENTRAL MEMORY T CELLS [TCM]:
express lymph node homing receptors and thus stay in the
lymph nodes. CD45RO+CD45RA- CCR7+ Have no
effector function. They stimulate dendritic cells to produce
IL-12 upon secondary stimulation and differentiate into
CCR7- cells.
2. EFFECTOR MEMORY T CELLS [TEM]:
CD45RO+CD45RA- CCR7- develop receptors to migrate
to the inflamed tissues (e.g. CLA in the skin). express
receptors for migration to inflamed tissues and have
immediate effector function.
Memory T cells
41.
After recognition of the antigen
CD4: T helper cells (Th):
activate the immune system to combat the antigen
including both T and B cells.
CD8: T cytotoxic cells (Tc):
Antiviral and anti-tumor responses
Effector T cell function
42.
According to the type of antigen recognized by the
Th cells they secrete different cytokine patterns that
will further stimulate different parts of the immune
system.
Pre-activated precursor Th cells (Th0) secretes a
wide variety if cytokines which then develops into:
Th1 or Th2 with more restricted type of cytokine
secretion.
T helper response
43.
44.
45. Th1 cells Th 2 cells
Differentiation from Th0
mediated by
IL-12 IL-4
Secretes
a) IL-2: stimulates both
Th and Tc
proliferation.
b) IFN GAMMA:
activates
macrophages and NK
cells and IL-12.
a) IL-4: Stimulates B cells
to produce IgE and
stimulates further Th 2
response and inhibits
Th1 response.
b) IL-5: promotes
eosinophil growth.
c) IL-10: inhibits Th1
response
Mediates
CELL MEDIATED
RESPONSE
HUMORAL IMMUNITY
Th1 cells versus Th2
cells
47.
1. Depends mainly upon the type of antigen presented.
2. The cytokines it stimulates.
3. The Dendritic cells.
4. the toll like receptor.
5. Dose of antigen.
6. Genetic background of the host.
7. The APC and its cytokines.
8. The co-stimulatory molecules.
Th1/Th2 decision
49.
CD4 + T cells.
Secretes large amounts of IL-10.
Suppressor effect on both immune
responses.
Produced by immature inactive dendritic
cells.
Important for TOLERANCE towards self
antigens and regulating inflammation.
Regulatory T cells (Tregs)
52. Direct killing of the organism or the abnormal or infected cells.
TC1 and TC2 in cytokine patterns (functional roles still remain to
be determined. Even).
Viral and anti-tumor activities.
Cytotoxic T cells with CD8 surface protein are called CD8+ T cells.
Three different pathways of killing:
a) Perforin which forms pores in the target cell's plasma
membrane this causes ions and water to flow into the target
cell, making it expand and eventually lyse then Granzyme
that can enter target cells via the perforin-formed pore and
induce apoptosis.
b) Tc cells activate the death receptor Fas on the target cell by
expressing the cognate death ligand FasL. The activated Fas
also triggers apoptosis.
c) Cytokines, including TNF-α and IFN-γ, which are released as
long as TCR stimulation continues. These mediators can
affect distant cells as well as the target cell
Cytotoxic T cells (CD8+ T
cells)
53.
54.
B cells function to protect the host by producing
antibodies that identify unique antigen and neutralize
specific pathogens.
B Cells are the major cells involved in the creation of
humoral immunity.
Like the T cell receptor, B cells express a unique B
cell receptor (BCR), in this case, an immobilized
antibody molecule. The BCR recognizes and binds to
only one particular antigen.
Differentiates into an effector cell, known as a
PLASMA CELL
The B lymphocyte (B cells)
56.
T cell B cell
Antigens
reorganization
Processed form
in the context of an
MHC
Native form
Activation signals Th1 Th2
B cell Vs. T cell
ACTIVATION
57.
Short lived cells (2-3 days) which secrete antibodies
that bind to antigens, making them easier targets for
phagocytes, and trigger the complement cascade.
About 10% of plasma cells will survive to become
long-lived antigen specific memory B cells primed to
produce specific antibodies and respond quickly if
the same pathogen re-infects the host; while the host
experiences few, if any, symptoms.
Plasma cells
58.
Primary immune response – cellular differentiation
and proliferation, which occurs on the first exposure
to a specific antigen
Lag period: 3 to 6 days after antigen challenge.
Peak levels of plasma antibody are achieved in 10
days.
Antibody levels then decline.
Immunological Memory
59.
Secondary immune response – re-exposure to the
same antigen
Sensitized memory cells respond within hours.
Antibody levels peak in 2 to 3 days at much higher
levels than in the primary response.
Antibodies bind with greater affinity, and their levels in
the blood can remain high for weeks to months.
Immunological Memory
63.
Antibodies (or immunoglobulin, Ig), are large Y-
shaped proteins used by the immune system to
identify and neutralize foreign objects.
In mammals there are five types of antibody: IgA,
IgD, IgE, IgG, and IgM, differing in biological
properties, each has evolved to handle different
kinds of antigens.
Heavy chains: The heavy chains of a given antibody
molecule determine the class of that antibody: IgM(
μ), IgG(γ ), IgA(α ), IgD( δ), or IgE(ε ).
Antibodies
64. IgG is monomer Ig & the most abundant
immunoglobulin, accounting for approximately 75%
of the total amount of serum immunoglobulin.
The major immunoglobulin of the secondary immune
response.
Four subclasses (IgG1, IgG2, IgG3, IgG4) are
defined by the amino acid sequences of their
constant region.
Most of the autoimmune dermatoses caused by
autoantibodies are mediated by IgG, most often
IgG4.
Crosses the placenta and confers passive immunity.
Immunoglobulin G
65.
The largest immunoglobulin.
IgM molecules are pentamers that (in addition to light
and heavy chains) contain one J chain.
IgM is the major immunoglobulin produced in the
primary immune response.
Upon binding to its antigen, IgM induces
agglutination and activates the classical complement
pathway.
Immunoglobulin M
66.
IgA is the predominant immunoglobulin present in
mucosal surfaces prevent attachment of pathogens to
epithelial cell surfaces.
IgA can activate the complement system via the
alternative (but not the classical) pathway.
Two subclasses of IgA exist, IgA1 and IgA2. IgA
molecules can be joined by a J chain; this dimer form is
mostly found in secretions, while in the serum, IgA
circulates primarily as a monomer.
IgA molecules can be involved in the pathogenesis of
bullous autoimmune diseases.
Immunoglobulin A
67.
IgE monomer is the classic anaphylactic antibody that
mediates most immediate allergic and anaphylactic
reactions.
Mast cells and basophils express high-affinity receptors
for the Fc portion of IgE (FcεRI). Antigens, anti-IgE
antibodies or other substances that crosslink at least two
IgE molecules bound on mast cells induce the release of
mediators.
Also LCs, dermal DCs and peripheral blood DCs as well
as monocytes from atopic individuals can bind monomeric
IgE via the high-affinity FcεRI.
The second IgE receptor, FcεRII exhibits weaker binding
affinity and is expressed on macrophages, eosinophils,
platelets, and particular subtypes of T and B cells.
Immunoglobulin E
68.
The function of IgD still remains mysterious. Recent
evidence suggests that IgD participates in respiratory
immune defense.
It binds to basophils and mast cells, stimulating their
production of antimicrobial factors.
IgD may also exert proinflammatory functions, as
illustrated by the hyperimmunoglobulinemia D with
periodic fever syndrome (HIDS).
Immunoglobulin D
76. Type I Hypersensitivity
Immediate (Anaphylactic type)
The reaction occurs within minutes after exposure
to an antigen.
Plasma cells produce IgE.
IgE causes mast cells to release histamine,
causing increased dilation and permeability of
blood vessels and constricting smooth muscle in
bronchioles of the lungs.
The reaction may range from hay fever to asthma
and life-threatening anaphylaxis.
77. When a specific antigen binds to mast cell-bound IgE,
the FcεRI becomes activated, which leads to
degranulation and release of preformed mediators,
including:
1. Histamine
2. Bradykinin
3. Serotonin.
4. Prostaglandins
5. Leukotrienes (B4, C4, D4 and E4),
6. Platelet activating factor
They enhance
i. vascular permeability
ii. bronchoconstriction
iii. induction of an inflammatory response
Type I Hypersensitivity
79. Type II Hypersensitivity
Cytotoxic type (Sub acute type)
Antibody combines with an antigen bound to the
surface of tissue cells, usually a circulating RBC.
Activated complement components, IgG and IgM
antibodies in blood, participate in this type of
hypersensitivity reaction.
This destroys the tissue that has the antigens on
the surface of its cells (e.g., Rh incompatibility).
80. Type III Hypersensitivity
Immune complex type (serum
sickness, SLE) (Also a Sub acute
type)
Immune complexes are formed between
microorganisms and antibody in circulating blood.
These complexes leave the blood and are
deposited in body tissues, where they cause an
acute inflammatory response.
Tissue destruction occurs following phagocytosis
by neutrophils.
81. Type IV Hypersensitivity
Cell-mediated type (delayed)
T lymphocytes that previously have been
introduced to an antigen cause damage
to tissue cells or recruit other cells.
Responsible for the rejection of tissue
grafts and transplanted organs
Allergic contact dermatitis.
82. The body produces auto-antibodies and sensitized TC cells
that destroy its own tissues
Examples include:
systemic lupus erythematosus (SLE)
Pemphigus
Autoimmune Diseases
83.
Dr Samia Esmat Professor of Dermatology Cairo
University
Bolognia: Dermatology, 2nd &3rd ed.
Immense Immunology Insight
Immunity and the immune system Dr. Angelo Smith
WHPL
References