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positive induction apoptosis 585 post-streptococcal glomerulonephritis<br />

Rodney Robert Porter.<br />

Paul Jules Portier.<br />

HLA molecules on allogeneic donor cells in the blood of a<br />

transplant recipient.<br />

positive induction apoptosis<br />

Two central pathways lead to apoptosis: (1) positive induction<br />

by ligand binding to plasma membrane receptor; and (2)<br />

negative induction by loss of suppressor activity. Each leads<br />

to activation of cysteine proteases with homology to IL1β<br />

converting enzymes (ICEs or caspases). Positive induction<br />

involves ligands related to TNF. Ligands are typically<br />

trimeric and bind to cell surface receptors causing aggregation<br />

(trimerization) of cell surface receptors. Receptor<br />

oligomerization orients their cytosolic death domains into<br />

a configuration that recruits adaptor proteins. The adaptor<br />

complex recruits caspase-8. Caspase-8 is activated, and the<br />

cascade of caspase-mediated disassembly proceeds.<br />

positive selection<br />

Pathway in the thymus that promotes the survival of<br />

immature T cells with receptors that recognize self<br />

peptide complexed to self MHC with only low affinity/<br />

avidity, i.e., those with the greatest capacity to identify<br />

nonself peptide complexed to self MHC with high affinity.<br />

Positively selected cells are the only ones permitted to<br />

continue their maturation. The resulting cell population is<br />

self MHC-restricted and capable of interacting with both<br />

self and foreign antigens. NKT cells are also subjected<br />

to positive selection in the thymus. It is unclear whether<br />

developing B cells with low affinity for self antigen<br />

receive survival signals, i.e., are positively selected. Refer<br />

to negative selection.<br />

postcapillary venules<br />

Relatively small blood vessels lined with cuboidal epithelium<br />

through which blood circulates after it exits capillaries<br />

and before it enters veins. They are frequent sites of migration<br />

of lymphocytes and inflammatory cells into tissues<br />

during inflammation. Recirculating lymphocytes migrate<br />

from the blood to lymph through high endothelial venules<br />

of lymph nodes.<br />

post-cardiotomy syndrome<br />

A condition that follows heart surgery or traumatic injury.<br />

Autoantibodies against heart antigens may be demonstrated<br />

by immunofluorescence within weeks of the surgery or<br />

trauma. Corticosteroid therapy represents an effective<br />

treatment. Patients suffering myocardial infarcts may also<br />

develop a similar condition.<br />

post-GC<br />

Designation for a leukemia/lymphoma in which the transformed<br />

cells express an activated B cell or memory B cell<br />

phenotype. There is a high frequency of somatic hypermutations<br />

in the genome.<br />

post-infectious encephalomyelitis<br />

Demyelinating disease following a virus infection that is<br />

mediated by autoimmune delayed-type (type IV) hypersensitivity<br />

to myelin.<br />

post-infectious iridocyclitis<br />

Inflammation of the iris and ciliary body of the eye. This<br />

may occur after a virus or bacterial infection and is postulated<br />

to result from an autoimmune reaction.<br />

post-rabies vaccination encephalomyelitis<br />

A demyelinating disease produced in humans actively<br />

immunized with rabies vaccine containing nervous system<br />

tissue to protect against the development of rabies. Serial<br />

injections of rabbit brain tissue containing rabies virus<br />

killed by phenol may induce demyelinating encephalomyelitis<br />

in a recipient. This method of vaccination was<br />

replaced with a vaccine developed in tissue culture that did<br />

not contain any nervous tissue.<br />

post-streptococcal glomerulonephritis<br />

An acute proliferative glomerulonephritis that may<br />

follow a streptococcal infection of the throat or skin by 1<br />

to 2 weeks. It is usually seen in 6- to 10-year old children,<br />

but may occur in adults as well. The onset is heralded<br />

by acute nephritis. Ninety percent of patients have been<br />

infected with group A β hemolytic streptococci that are<br />

nephritogenic— specifically, types 12, 4, and 1, that are<br />

revealed by their cell wall M protein. Poststreptococcal<br />

glomerulonephritis is mediated by antibodies induced by<br />

the streptococcal infection. Most patients show elevated<br />

antistreptolysin-O (ASO) titers. Serum complement levels<br />

are decreased. Immunofluorescence of renal biopsies<br />

demonstrates granular immune deposits that contain<br />

immunoglobulin and complement in the glomeruli.<br />

This finding is confirmed by electron microscopy. The<br />

precise streptococcal antigen has never been identified;<br />

P

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