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22 Cards in this Set
- Front
- Back
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How to classify autoimmune disease |
A. mechanism by which loss of tolerance has occured B. presence and effects of autoantibodies C. extent to which different organs the body are affected by disease: i. tissue specific - affecting single/few organs ii. systemic - affecting multiple organs |
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Mechanisms of loss of tolerance |
1.Ignorance 2.T reg cells failing to suppress self-reactive T helper cells 3.Inappropriate antigen presentation |
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Mechanisms of loss of tolerance: Ignorance |
eye testis invisible to immune system mechanisms to suppress/remove reactive T helper cells local example of when ignorance goes wrong: sympathetic ophthalmia |
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Systemic ophthalmia |
penetrating injury to eye immune response to ipsilateral eye tissue also immune response to contralateral eye tissue → rapid vision loss |
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Mechanisms of loss of tolerance: T reg cells |
failure to suppress self reactive T helper cells → autoimmunity in RA Treg numbers normal, suppressive function of these cells is ↓ → atuoreactive cells escape from regulatory control |
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Mechanisms of loss of tolerance: Inappropriate antigen presentation pathogen mimics self proteins, immune system attacks pathogen and host tissue is attacked |
normally immune response to self antigens does not occur as T helper cells which are presented with cognate self-antigen do not get accompanying danger signals → anergy or apoptosis of T helper immunocompetent T + B cells which recognise self antigen and need T cell help to be activated are unable to respond in autoimmunity appearance of new antigenic determinant new antigenic determinant in association with self-antigen reactive T + B cells |
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inducing autoimmune disease |
adjuvants are substance adjuvants can be used to present self antigen to the T cells dead bacteria make good adjuvants as they give danger signals to costimulate dendritic cells → fully activate T cells |
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mechanism for breaking tolerance |
infectious agent makes protein peptide that mimics self protein infection can activate T cells because of danger signals then → self destruction to the host tissue |
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Presence + effects of autoantibodies: clones of lymphocytes |
breakdown of self tolerance → activation of clones of self reactive T + B cells autoimmune disease = autoAb |
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Goodpasture''s syndrome |
autoAb to basement membrane in kidney and lung |
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RA |
AutoAb to Fc portion of IgG |
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Myasthenia gravis |
AutoAb to AChR |
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do Ab → autoimmune disease? or does autoimmune disease → Abs being found? |
Autoimmune haemolytic anaemia Abs to RBC → haemolytic MI Ab to the heart are 2º to MI |
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Mechanisms by which AutoAb can produce autoimmune disease |
1. complement dependent lysis 2. opsonisation 3. formation of immune complexes 4. blockade of receptor for physiological ligands 5. stimulation of cell surface receptors |
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mechanisms by which autoAb produce autoimmune disease: complement dependent lysis |
Paroxysmal cold Haemoglobinuria auto immune complement-fixing IgG antibodies → Haemoglobinuria |
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mechanisms by which autoAb produce autoimmune disease: opsonisation |
haemolytic anaemias density of Ig is insufficient to allow cross linking and activation of C1q |
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mechanisms by which autoAb produce autoimmune disease: formation of immune complexes |
Glomerulonephritis in SLE in SLE get multiple autoAb -ve charge of glomerulus basement membrane +ve charge immune complexes accumulate there |
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mechanisms by which autoAb produce autoimmune disease: Blockade of receptor for physiological ligands |
Myasthenia graves - AutoAb to AChR Pernicious anaemia - AutoAb to IF/gastric parietal cells |
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mechanisms by which autoAb produce autoimmune disease: stimulation of cell surface receptors |
Grave's disease antibodies mimic actions of TSH at thyroid gland |
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examples of tissue specific autoimmunity: Thyroid + ocular connective tissue Kidney/lung basement membrane β cells of pancreas Parietal cells/IF Adrenal glands AChR |
Grave's, Hashimoto's
Goodpasture's syndrome DM Pernicious anaemia Addison's disease Myasthenia graves |
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RA |
systemic inflammatory disease AutoAb to Fc portion of IgG (Rheumatoid factor) + AutoAb to citrullinated proteins (anti-CCP Abs) Women>Men affects hands, wrists, feet mostly systemic: lung fibrosis, vasculitis, ulceration, gangrene, permanent eye damage, nerve damage Patients +ve for Rheumatoid factor + Anti CCP Abs → ↑ risk of joint erosion smoking risk factor for developing RA in patients with specific genetic backgrounds e.g. genes coding for certain MHC II (HLA-DRB1) environmental factors> genetic Citrullination - normal process but associated with inflammation |
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genetic input for autoimmunity |
most autoimmune disease have both genetic + environmental components |
