hypersensitivity, allergy and inflammation Flashcards
immunological mechanisms: summarise the mechanisms by which IgE, antibodies, immune complexes and T cells can cause tissue damage and inflammation (the four types of hypersensitivity); clinical disease: list examples of the clinical syndromes associated with each type of hypersensitivity reaction
what do appropriate immune responses occur in response to
harmful agents e.g. viruses, bacteria, fungi, parasites
function and side effect of appropriate immune response
eliminate pathogens, and whilst there may be concomitant tissue damage as a side effect, as long as pathogen is eliminated quickly this will be minimal and repaired easily
what 2 thnigs does appropriate immune response involve
recognition by cells of immune system and antibody production
what does appropriate immune tolerance occur in response to
self and to foreign harmless proteins e.g. food, pollens, other plant proteins, animal proteins, commensal bacteria
what does appropriate immune tolerance involve
antigen recognition and generation of Treg cells and regulatory (blocking) antibody (IgG4) production (antigen recognition in context of danger signals (microbial signatures) leads to immune reactivity, but in absence of danger leads to tolerance)
what 3 things do immune responses mount against to cause hypersensitivity reactions
harmless foreign antigens (allergy, contact hypersensitivty), autoantigens (autoimmune diseases), alloantigens (serum sickness, transfusion reactions, graft rejection)
4 classes of hypersensitivity reactions (many diseases involve mixture of types)
type I: immediate hypersensitivity (IgE), type II: antibody-dependent cytotoxicity hypersensitivity (antibody), type III: immune complex mediated hypersensitivity (complex), type IV: delayed cell mediated hypersensitivity (T cell)
type I: what is immediate hypersensitivity present in
anaphylaxis, asthma, rhinitis (seasonal and perennial), food allergy
type I: immediate hypersensitivity: 3 features and purposes of primary antigen exposure
sensitisation not tolerance, IgE antibody production, IgE binding to mast cells and basophils
type I: immediate hypersensitivity: 3 features of secondary antigen exposure
more IgE antibodies produced, antigen exposure causes cross-linking IgE on mast cells and basophils, IC signalling leading to degranulation and release of inflammatory mediators
type II: antibody-dependent hypersensitivity: what does clinical presentation depend on
target tissue (i.e. organ-specific)
type II: antibody-dependent hypersensitivity: 4 organ-specific autoimmune diseases and what antibodies do to cause them
myasthenia gravis (anti-acetylcholine receptor antibodies), glomerulonephritis (anti-glomerular basement membrane antibodies), pemphigus vulgaris (anti-epithelial cell cement protein antibodies), pernicious anaemia (intrinsic factor blocking antibodies)
type II: antibody-dependent hypersensitivity: what happens in autoimmune cytopenias
antibody mediated blood cell destruction
type II: antibody-dependent hypersensitivity: 3 autoimmune cytopenias
haemolytic anaemia, thrombocytopenia, neutropenia
type II: antibody-dependent hypersensitivity: 2 tests for specific antibodies
immunofluorescence, ELISA (e.g. anti-CCP for rheumatoid arthritis)