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===See [[Autoimmune diseases - WikiClinical#Autoimmune diseases|here]]===
==Introduction==
'''Autoimmune disease''' is defined as ''a disease state characterized by a specific antibody or cell mediated response against the body's own tissues ('self' antigens).
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'.
Particular individuals may be more susceptible to autoimmune diseases due to:
===Genetic factors===
Many autoimmune diseases have a familiar component and the Human Leucocyte Antigen (HLA) haplotype is the prodomient genetic factor, however having a particular HLA haplotype does not automatically result in the development of an autoimmune disease.
* HLA-DR3/DR4 (MHC Class II):
1. Diabetes Mellitus
2. Rheumatoid Arthritis
* HLA-B27 (MHC Class I):
1. Ankylosing spondylitis
* TNF alpha
* CTLA-4
===Hormonal factors===
Testosterone is protective against Systemic Lupus Erythematosus (SLE) and thus it is not seen in males.
===Environmental factors===
'''''Infection'''''
1. Molecular mimicry
* Some bacteria and viruses have antigens that resemble host-cell components and the body then also can initiate an immune response against itself.
2. Polyclonal activation
* T and B cells activation can occur as a result of an infection resulting in polyclonal activation. This can then cause autoreactive autoantibodys or mediate autoimmunity.
3. Inappropriatee MHC expression
* Autoreactive T cells are activated because infection stimulates APC and upregulates MHC class II.
'''''Diet'''''
'''''Stress'''''
{| border="1" cellpadding="2"
!width="150"|
!width="150"|Antibody mediated
!width="50"|Antibody mediated
!width="200"|Cell mediated
|-
| '''Type of hypersensitivity''' || [[Type II Hypersensitivity - WikiBlood|Type II]] || [[Type III Hypersensitivity - WikiBlood|Type III]] || [[Type IV Hypersensitivity - WikiBlood|Type IV]]
|-
| '''Pathogenesis''' || Antibody to cell surface or matrix antigens || Antibody to soluble self antigens || T cell and macrophage activation to self antigens
|-
| '''Examples of diseases''' || Immune mediated haemolytic anaemia (IMHA) || Systemic Lupus Erythematosus (SLE) || Rheumatoid arthritis
|-
| || Immune mediated thrombocytopaenia (IMTP)|| || Diabetes Mellitus type 1
|-
| || Myasthenia gravis || || Hypothyroidism (lymphocytic throiditis)
|-
| || Pemphigus Vulgaris || || Hypoadrenocorticism (Addisons disease)
|-
| || Bullous pemphigoid || ||
|}
==Antibody mediated autoimmune diseases==
[[Image:Large.jpg|right|thumb|150px|Myasthenia gravis - From Immunity: The Immune Response in Infectious and Inflammatory Disease DeFranco, Locksley and Robertson New Science Press 1999-2007]]
===1. Immune Mediated Haemolytic Anaemia (IMHA)===
'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|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 - WikiBlood|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 - WikiBlood|Type II hypersensitivity]]
===4. Bullous Pemphigoid===
'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|Type II hypersensitivity]]
===5. Pemphigus Vulgaris===
'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|Type II hypersensitivity]]
===6. Systemic Lupus Erythematosus (SLE)/Multi-systemic immune mediated disease===
'''Pathogenesis:''' [[Type III Hypersensitivity - WikiBlood|Type III hypersensitivity]]
==Cell mediated autoimmune diseases==
[[Image:Rheumatoid Arthritis Type IV hypersensitivity.jpg|right|thumb|150px|Rheumatoid Arthritis-Brian Catchpole RVC 2008]]
[[Image:Diabetes Mellitus Type IV hypersensitivity.jpg|right|thumb|150px|Diabetes Mellitus-Brian Catchpole RVC 2008]]
===1. Rheumatoid arthritis===
'''Pathogenesis:'''
* [[Type IV Hypersensitivity - WikiBlood|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 - WikiBlood|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 - WikiBlood|Type IV hypersensitivity]]
* T cell mediated
===4. Hypoadrenocorticism (Addisons disease)===
'''Pathogenesis:''' [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]
==References==