Difference between revisions of "Autoimmune Diseases - Introduction"
| (5 intermediate revisions by the same user not shown) | |||
| Line 3: | Line 3: | ||
'''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). | '''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). | ||
| − | The breakdown of [[Immune Tolerance|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'. | + | 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: | Particular individuals may be more susceptible to autoimmune diseases due to: | ||
| Line 55: | Line 55: | ||
!width="200"|Cell mediated | !width="200"|Cell mediated | ||
|- | |- | ||
| − | | '''Type of hypersensitivity''' || [[Type II Hypersensitivity|Type II]] || [[Type III Hypersensitivity|Type III]] || [[Type IV Hypersensitivity|Type IV]] | + | | '''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 | | '''Pathogenesis''' || Antibody to cell surface or matrix antigens || Antibody to soluble self antigens || T cell and macrophage activation to self antigens | ||
| Line 65: | Line 65: | ||
| || [[Myasthenia Gravis|Myasthenia gravis]] || || [[Hypothyroidism]] (lymphocytic throiditis) | | || [[Myasthenia Gravis|Myasthenia gravis]] || || [[Hypothyroidism]] (lymphocytic throiditis) | ||
|- | |- | ||
| − | | || [[Pemphigus]] || || [[Hypoadrenocorticism]] (Addisons disease) | + | | || [[Pemphigus Vulgaris]] || || [[Hypoadrenocorticism]] (Addisons disease) |
|- | |- | ||
| || [[Bullous Pemphigoid]] || || | | || [[Bullous Pemphigoid]] || || | ||
|} | |} | ||
| − | + | ||
| − | |||
[[Category:Autoimmune Diseases]] | [[Category:Autoimmune Diseases]] | ||
Revision as of 15:15, 11 August 2010
Introduction
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).
The breakdown of 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 predominant 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 can then also 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 autoantibodies or mediate autoimmunity.
3. Inappropriate MHC expression
- Autoreactive T cells are activated because infection stimulates APC and upregulates MHC class II.
Diet
Stress
| Antibody mediated | Antibody mediated | Cell mediated | |
|---|---|---|---|
| Type of hypersensitivity | Type II | Type III | 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|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 |