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IgCAMs

Don't require Ca2+. Have Ig motif

Monoclonal antibodies

Inject human leukocytes into mice, mice develop antibodies against, Removed spleen and picked only cells that were involved in cell cell adhesion. This is how they Identified the cell adhesion families

IgCAMs (3)

1. ICAM 1,2,3 - important bc on endothelium, upregulated during inflammatory response.
2. CD2 - on T cells, binds LFA-3 on APCs 3. LFA-3 on APCs, binds CD2 on T cells.

Integrins (4) (Ca+2)

B1 - VLA family - found on many cells, binds extracellular matrix and allows for migration through extracellular matrix
B2 - (3 kinds) 1. LFA-1 (CD11a/CD18), expressed by most leukocytes - binds ICAM 1,2,3 of endothelium. 2. CR3 (CD18/CD11b) - on phagocytes. Binds ICAM-1 and C3b so, binds to endothelim and is a opsonin receptor. CR4 (CD18/CD11c) on phagocytes, bind iC3b opsinin -> phagocytosis.

Leukocyte Adhesion Def (3 CCs

No beta chain of B2 integrins -> Decreased opsinization = increased infection with encapsulated bacteria, defective chemotaxis- bc cant bind and cross endothelium, lymphocyte function (eg. CTL killing doesnt req. integrins) usually normal. If you see bacteria but no white cells accumulating, that means they leukocytes cant adhere to endothelium (no LFA-1 and CR3) and move to site of infection. NO matter what chemotaxis are present, it doesn't matter bc the leukocytes cant adhere in the first place. IMP for Board EXAMS

Selectins (3)

Lectin = any molecule that can bind a carbohydrate. L-selectin - leukocyte selectin -> L selectins on leukocytes attach to high endothelial venules of lymph nodes, they recognize the carbohydrates and bind selectively to lymph node venules. E-selectin - found on endothelium - bind to carbohydrates on leukocytes, initiates rolling, aren't expressed unless they need to recruit leukocytes. Activation by proinflamatory cytokines (IL -1, IL-6, TNF-alpha) released by macrophages after encountering antigen. These cytokines also pull endotheilial cells apart for extravasion. EP - selectin - found on platelets, and endothelial cells - same function as E-selectin

Cadherins

Ca2+ dependent. Like cell to like cell binding. E- cadherin = epithelial cell to epithelial cell. N caderhin = neural cell to neural cell. No role in immune function.

Acute Phase

Period during physiological changes of inflammation. Macrophages release IL-1,6,8 and TNF alpha. Leads to pro inflammatory events. IL -6 -> Mannose binding protein, C - reactive protein-> act as opsinins

Erythrocyte Sedimentation Rate

Is a nonspecific indicator of inflammation. Due to activation of fibrinogen which binds to RBCs, partially neutralizing its negative charge. They then stick to each other and stack up. The stacks sediment more quickly than unstacked cells.

Acute Phase Blood Protein Changes

CRP and Serum Amyloid A (SAA) rise several hundred fold. Just know CRP. Albumin decreases. Fibrinogen and C3 rise less percentage wise compared to CRP but do contribute to the response.

CRP

planar pentamer. Binds to pneumoccal C polysaccharide, Phosphorylcholine - exposed on damaged cells, binds nuclear constitutients, binds to C1q and activates compliment without a ligand, binds to Fcgamma receptors (same receptor IgG binds) on phagocytes mediating particle uptake, is therefore, an opsinin. Does a lot of the things IgG does.

CRP levels

are an indicator of MI, not highly specific but can be a marker.

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