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Cytokines and Allergies


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Lymphokines
are cytokines secreted by lymphocytes (Tcells)
Monokines
are cytokines secreted by mononuclear phagacytes (eg. macrophages)
Interleukins
are cytokines secreted by Tcells that affect other leukocyte populations
Chemokines
are cytokines involved in chemotaxis
Pleiotropy
is the ability of a cytokine (or protein, gene) to exert different effects on different target cells
Redundancy
is when two or more cytokines (or protein, gene) exert similar effects
Synergy
is when the combined effect of cytokines (or proteins, genes) is greater than the sum of individual effects
Biological cascades
may be induced as small molecules (eg. cytokines) initiate chemical pathways
Haematopoietins
are growth/differentiation factors affecting the differentiation of haematopoietic stem cells to immune cells
Tumour necrosis factors
are a large family of cytokines (>17) that exhibit anti-tumour cell activity and mediate inflammation
High affinity
of cytokine to receptor means that only small amounts are required to stimulate a response
Type 1 hypersensitivity
IgE binds to mast cells causing degranulation of histamine (eg. anaphylactic allergies)
Type 2 hypersensitivity
IgG and IgM damage cells by inducing phagocytosis (opsonisation) or lysis (eg. blood transfusions)
Type 3 hypersensitivity
insolube IgG/M-antigen complexes deposit in tissues activating complements, causing inflammation and tissue damage (eg. rheumatoid arthritis)
Type 4 hypersensitivity
TH1 cells are sensitised and activate CD8 Tcells/macrophages to cause cell death in response to large, insluble antigens (eg. organ transplant) (not Ig mediated)
Corticosteroids and β2 agonists
are anti-inflammatories and bonchodilators respectively, used to treat asthma
Bronchoconstriction
in asthma is due to increased responsiveness to non-specific spasmogens (eg. histamine)
Asthma
is characterized by mucus plugging, inflammation and bronchoconstriction causing reversible airway obstruction
Mast cells and basophils
mediate early phase asthma response as IgE-dependent degranulation releases histamine, prostaglandin and leukotrienes causing bronchoconstriction.
Tcells and eosinophils
mediate late phase asthma response called airway hyper reactivity (AHR) in which IL-4,5,13 amplify the TH2 response (=recruit granulocytes)
Chronic asthma
results from inflam. induced remodelling of lung including thickening of sub-epithelial membrane, increased smooth muscle mass and sub-epithelial collagen deposites (fibrosis)