Difference between revisions of "Category:Autoimmune Diseases"

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==Introduction==
 
  
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'''Autoimmune disease''' is defined as ''a disease state characterised by a specific antibody or cell mediated response against the body's own tissues ('self' antigens).
 
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The breakdown of [[Immune Tolerance - WikiBlood|tolerance]] to self antigens and the failure to regulate pathological immune responses are both responsible for autoimmune diseases. It has been shown in mice that thymectomy causes autoimmune disease, and plays a very important role in the recognition of 'self'.
 
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Particular individuals may be more susceptible to autoimmune diseases due to:
 
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===Genetic factors===
 
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Many autoimmune diseases have a familiar component and the Human Leucocyte Antigen (HLA) haplotype is the predominant genetic factor, however having a particular HLA haplotype does not automatically result in the development of an autoimmune disease.
 
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* HLA-DR3/DR4 (MHC Class II):
 
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1. Diabetes Mellitus
 
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2. Rheumatoid Arthritis
 
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* HLA-B27 (MHC Class I):
 
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1. Ankylosing spondylitis
 
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* TNF alpha
 
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* CTLA-4
 
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===Hormonal factors===
 
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Testosterone is protective against Systemic Lupus Erythematosus (SLE) and thus it is not seen in males.
 
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===Environmental factors===
 
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'''''Infection'''''
 
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1. Molecular mimicry
 
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* Some bacteria and viruses  have antigens that resemble host-cell components and the body can then also initiate an immune response against itself.
 
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2. Polyclonal activation
 
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* T and B cells activation can occur as a result of an infection resulting in polyclonal activation. This can then cause autoreactive autoantibodies or mediate autoimmunity.
 
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3. Inappropriate MHC expression
 
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* Autoreactive T cells are activated because infection stimulates APC and upregulates MHC class II.
 
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'''''Diet'''''
 
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'''''Stress'''''
 
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{| border="1" cellpadding="2"
 
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!width="150"|
 
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!width="150"|Antibody mediated
 
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!width="50"|Antibody mediated
 
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!width="200"|Cell mediated
 
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|-
 
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| '''Type of hypersensitivity''' || [[Type II Hypersensitivity - WikiBlood|Type II]] || [[Type III Hypersensitivity - WikiBlood|Type III]] || [[Type IV Hypersensitivity - WikiBlood|Type IV]]
 
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|-
 
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| '''Pathogenesis''' || Antibody to cell surface or matrix antigens  || Antibody to soluble self antigens || T cell and macrophage activation to self antigens
 
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| '''Examples of diseases''' || Immune mediated haemolytic anaemia (IMHA)  || Systemic Lupus Erythematosus (SLE) || Rheumatoid arthritis
 
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|-
 
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|  || Immune mediated thrombocytopaenia (IMTP)||                          || Diabetes Mellitus type 1
 
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|-
 
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|  || Myasthenia gravis  ||  || Hypothyroidism (lymphocytic throiditis)
 
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|-
 
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|  || Pemphigus Vulgaris  ||  || Hypoadrenocorticism (Addisons disease)
 
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|-
 
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|  || Bullous pemphigoid  ||  ||
 
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|}
 
  
 
==Antibody mediated autoimmune diseases==
 
==Antibody mediated autoimmune diseases==

Revision as of 14:46, 11 August 2010


Antibody mediated autoimmune diseases

Myasthenia gravis

1. Immune Mediated Haemolytic Anaemia (IMHA)

Pathogenesis: Type II hypersensitivity

  • Autoantibody attack on the red blood cells causing extravascular and intravascular lysis which causes anaemia.
  • The in saline autoagglutination test and the coombes test is used to diagnose the disorder.

2. Immune Mediated Thrombocytopaenia (IMTP)

Pathogenesis: Type II hypersensitivity

  • There is an immunological attack on the platelets which reduces the ability for clotting.
  • A reduced platelet count and detection of anti-platelet antibodies in the serum are used for diagnosis of this disorder.

3. Myasthenia gravis

Pathogenesis: Type II hypersensitivity

4. Bullous Pemphigoid

Pathogenesis: Type II hypersensitivity

5. Pemphigus Vulgaris

Pathogenesis: Type II hypersensitivity

6. Systemic Lupus Erythematosus (SLE)/Multi-systemic immune mediated disease

Pathogenesis: Type III hypersensitivity

Cell mediated autoimmune diseases

Rheumatoid Arthritis-Brian Catchpole RVC 2008
Diabetes Mellitus-Brian Catchpole RVC 2008

1. Rheumatoid arthritis

Pathogenesis:

  • Type IV hypersensitivity: CD4 Th-1 cell mediated.
  • Macrophages phagocytose self antigens and can present peptides on their MHC Class II molecules. The autoreactive TH-1 cells release IFN-gamma which activates macrophages to release prostaglandins, MMP enzymes and TNF-alpha (pro-inflammatory mediator), see diagram. These cytokines cause inflammation and tissue destruction.

2. Diabetes Mellitus type I

Pathogenesis:

  • Type IV hypersensitivity
  • The CTLs think that all the beta cells in the pancreas are infected by a virus, as it wrongly detects a self antigen presented by the MHC class I on the surface of the cell as foreign.
  • Autoreactive CD8+ CTLs are inadvertently activated, destroying the beta cells, thus preventing the secretion of insulin and causing diabetes type 1 (see diagram).

3. Hypothyroidism (lymphocytic throiditis)

Pathogenesis: Type IV hypersensitivity

  • T cell mediated

4. Hypoadrenocorticism (Addisons disease)

Pathogenesis: Type IV hypersensitivity

Subcategories

This category has the following 2 subcategories, out of 2 total.

A

C

Pages in category "Autoimmune Diseases"

This category contains only the following page.

A

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