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UNIVERSITY INSTITUTE OF BIOTECHNOLOGY
Master’s of Science (Bioinformatics)
Subject: Immunology and Immunoinformatics
Code:22BNT-725
Autoimmune disease
Course outcomes
CO1
Students will learn about vario us immune system components
CO2 Students will learn about HLA and immune responses
CO3 Students will be able to understand types of hypersensitivity and autoimmune disorders
CO4 Students will be able to explain various vaccination strategies and their limitations
CO5 Students will learn about immunoinformatics, its applications in vaccine design and various
immunological databases and tools
AUTOIMMUNITY
AND
AUTOIMMUNE DISEASES
T cell Development
Bone Marrow
Thymus
Lymph
Nodes
Spleen
In normal individuals, majority of lymphocytes
reacting with auto-antigens are deleted in primary
DELETION (Central
lymphoid organs by CLONAL
Tolerance)
Few self-reactive lymphocytyes which escape and
reach secondary lymphoid tissues are down regulated
there by CLONAL ANERGY
, Tregs or other
mechanisms (Peripheral Tolerance)
HORROR AUTOTOXICUS: Ehlrich proposed that
immune system should not be toxic to auto (self)
tissues.
Thus, normal
ANTIGENS
individuals are TOLERANT to AUTO
IDIOTYPE ANTI-IDOTYPE
ANTI-ANTI
IDIOTYPE
NEGATIVE SIGNAL
AUTOIMMUNITY: The presence of autoantibodies (antibodies against auto- antigens) or
autoreactive (self reactive) lymphocytes without the induction of any pathological changes
Autoantibodies can be found in normal individuals, particularly in old animals and in the
female gender group
AUTOANTIBODIES may have a physiological role in:
1. Removal of senescent/ damaged cells
2. Idiotype anti-idiotypes negative feed back
AUTOIMMUNE DISEASES: Pathological changes (structural and/or functional) in tissues
and/or organs as a consequence of autoreactive cells
CRITERIA FOR AUTOIMMUNE DISEASE OR WITEBSKY’S POSTULATES
1. The presence of autoantibodies or autoreactive lymphocytes ( in association
with pathological changes )
2. Experimental reproduction of the disease in laboratory animals
3. The features of the experimental disease must closely match with the
clinical disease.
4. Ability to passively transfer the disease by autoantibodies or lymphocytes
• Autoimmunity results from a failure or breakdown of the mechanisms normally
responsible for maintaining self-tolerance in B cells, T cells, or both.
• Although underlying molecular etiologies remain elusive for most autoimmune
diseases, it is thought that autoimmunity is multifactorial, resulting from a complex
interplay between genetic susceptibility, environmental triggers, and aberrant
immune regulation
• Autoimmune diseases may be either systemic or organ specific.
• Various effector mechanisms are responsible for tissue injury in different
autoimmune diseases.
• It is not uncommon for a patient to have symptoms of more than one autoimmune
disease (known as ‘overlap’, or undifferentiated collagen vascular syndrome).
• On contrary, a patient with one autoimmune disease may have serologic markers –
but no clinical manifestations – of another
General Characteristics
REFERENCES
• Kuby, Immunology II and V Edition.
8
Text Books
s Title Author Edition Year
Publisher
Name
T-1 Immunology Janis Kuby 5th 2002 W..Freeman
and company.
Kuby J (2002). Textbook of Immunology. W..Freeman and company.
THANKYOU
9

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1.3.6 Autoimmune disease.pptx

  • 1. UNIVERSITY INSTITUTE OF BIOTECHNOLOGY Master’s of Science (Bioinformatics) Subject: Immunology and Immunoinformatics Code:22BNT-725 Autoimmune disease
  • 2. Course outcomes CO1 Students will learn about vario us immune system components CO2 Students will learn about HLA and immune responses CO3 Students will be able to understand types of hypersensitivity and autoimmune disorders CO4 Students will be able to explain various vaccination strategies and their limitations CO5 Students will learn about immunoinformatics, its applications in vaccine design and various immunological databases and tools
  • 4. T cell Development Bone Marrow Thymus Lymph Nodes Spleen In normal individuals, majority of lymphocytes reacting with auto-antigens are deleted in primary DELETION (Central lymphoid organs by CLONAL Tolerance) Few self-reactive lymphocytyes which escape and reach secondary lymphoid tissues are down regulated there by CLONAL ANERGY , Tregs or other mechanisms (Peripheral Tolerance) HORROR AUTOTOXICUS: Ehlrich proposed that immune system should not be toxic to auto (self) tissues. Thus, normal ANTIGENS individuals are TOLERANT to AUTO
  • 5. IDIOTYPE ANTI-IDOTYPE ANTI-ANTI IDIOTYPE NEGATIVE SIGNAL AUTOIMMUNITY: The presence of autoantibodies (antibodies against auto- antigens) or autoreactive (self reactive) lymphocytes without the induction of any pathological changes Autoantibodies can be found in normal individuals, particularly in old animals and in the female gender group AUTOANTIBODIES may have a physiological role in: 1. Removal of senescent/ damaged cells 2. Idiotype anti-idiotypes negative feed back
  • 6. AUTOIMMUNE DISEASES: Pathological changes (structural and/or functional) in tissues and/or organs as a consequence of autoreactive cells CRITERIA FOR AUTOIMMUNE DISEASE OR WITEBSKY’S POSTULATES 1. The presence of autoantibodies or autoreactive lymphocytes ( in association with pathological changes ) 2. Experimental reproduction of the disease in laboratory animals 3. The features of the experimental disease must closely match with the clinical disease. 4. Ability to passively transfer the disease by autoantibodies or lymphocytes
  • 7. • Autoimmunity results from a failure or breakdown of the mechanisms normally responsible for maintaining self-tolerance in B cells, T cells, or both. • Although underlying molecular etiologies remain elusive for most autoimmune diseases, it is thought that autoimmunity is multifactorial, resulting from a complex interplay between genetic susceptibility, environmental triggers, and aberrant immune regulation • Autoimmune diseases may be either systemic or organ specific. • Various effector mechanisms are responsible for tissue injury in different autoimmune diseases. • It is not uncommon for a patient to have symptoms of more than one autoimmune disease (known as ‘overlap’, or undifferentiated collagen vascular syndrome). • On contrary, a patient with one autoimmune disease may have serologic markers – but no clinical manifestations – of another General Characteristics
  • 8. REFERENCES • Kuby, Immunology II and V Edition. 8 Text Books s Title Author Edition Year Publisher Name T-1 Immunology Janis Kuby 5th 2002 W..Freeman and company. Kuby J (2002). Textbook of Immunology. W..Freeman and company.