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#REDIRECT[[:Category:Autoimmune Diseases]]
 
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{{toplink
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|linkpage =WikiClinical
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|linktext =WikiClinical
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|maplink = WikiClinical Content Map
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|pagetype = Clinical
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|sublink1 = Immunology - WikiBlood
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|subtext1 = IMMUNOLOGY
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}}
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<br>
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==Introduction==
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'''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).
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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 prodomient 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 then also can 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 autoantibodys or mediate autoimmunity.
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3. Inappropriatee 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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|-
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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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|}
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==Antibody mediated autoimmune diseases==
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[[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]]
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===1. Immune Mediated Haemolytic Anaemia (IMHA)===
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'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|Type II hypersensitivity]]
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* Autoantibody attack on the red blood cells causing extravascular and intravascular lysis which causes anaemia.
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* The in saline autoagglutination test and the coombes test is used to diagnose the disorder.
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===2. Immune Mediated Thrombocytopaenia (IMTP) ===
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'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|Type II hypersensitivity]]
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* There is an immunological attack on the platelets which reduces the ability for clotting.
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* A reduced platelet count and detection of anti-platelet antibodies in the serum are used for diagnosis of this disorder.
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===3. Myasthenia gravis===
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'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|Type II hypersensitivity]]
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===4. Bullous Pemphigoid===
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'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|Type II hypersensitivity]]
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===5. Pemphigus Vulgaris===
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'''Pathogenesis:''' [[Type II Hypersensitivity - WikiBlood|Type II hypersensitivity]]
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===6. Systemic Lupus Erythematosus (SLE)/Multi-systemic immune mediated disease===
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'''Pathogenesis:''' [[Type III Hypersensitivity - WikiBlood|Type III hypersensitivity]]
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==Cell mediated autoimmune diseases==
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[[Image:Rheumatoid Arthritis Type IV hypersensitivity.jpg|right|thumb|150px|Rheumatoid Arthritis-Brian Catchpole RVC 2008]]
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[[Image:Diabetes Mellitus Type IV hypersensitivity.jpg|right|thumb|150px|Diabetes Mellitus-Brian Catchpole RVC 2008]]
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===1. Rheumatoid arthritis===
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'''Pathogenesis:'''
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* [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]: CD4 Th-1 cell mediated.
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* 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.
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===2. Diabetes Mellitus type I===
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'''Pathogenesis:'''
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* [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]
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* 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.
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* Autoreactive CD8+ CTLs are inadvertently activated destroying the beta cells thus preventing the secretion of insulin and causing diabetes type 1 (see diagram).
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===3. Hypothyroidism (lymphocytic throiditis)===
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'''Pathogenesis:''' [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]
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* T cell mediated
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===4. Hypoadrenocorticism (Addisons disease)===
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'''Pathogenesis:''' [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]
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==References==
 
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