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| − | {{review}}
| + | #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
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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 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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| − | | '''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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| − | | '''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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| − | | || Immune mediated thrombocytopaenia (IMTP)|| || Diabetes Mellitus type 1
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| − | | || Myasthenia gravis || || Hypothyroidism (lymphocytic throiditis)
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| − | | || Pemphigus Vulgaris || || Hypoadrenocorticism (Addisons disease)
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| − | | || Bullous pemphigoid || ||
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| − | |}
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| − | ==Antibody mediated autoimmune diseases==
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| − | [[Image:ImageNeeded.png|right|thumb|150px|Myasthenia gravis]]
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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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