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Untitled - D Ank Unlimited

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decomplementation 218 degranulation<br />

is absent from the red blood cells of paroxysmal nocturnal<br />

hemoglobulinuria patients. It facilitates dissociation of<br />

classical complement pathway C3 convertase (C4b2a) into<br />

C4b and C2a. It also promotes the dissociation of alternative<br />

complement pathway C3 convertase (C3bBb) into C3b<br />

and Bb. It inhibits C5 convertases (C4b2a3b and C3bBb3b)<br />

on the cell surface. DAF reacts with the convertases and<br />

destabilizes them by inducing rapid dissociation of a<br />

catalytic subunit C2a or Bb. The inhibitory effect of DAF<br />

is restricted to C3/C5 convertases bound to host cells; DAF<br />

does not inhibit normal complement activation on microbial<br />

or immune complex targets. DAF is found on selected<br />

mucosal epithelial cells and endothelial cells. It prevents<br />

complement cascade amplification on the surfaces of cells<br />

to protect them from injury by autologous complement. The<br />

physiologic function of DAF may be to protect cells from<br />

lysis by serum. DAF competes with C2 for linkage with<br />

C4b to block C3 convertase synthesis in the classical pathway.<br />

The DAF molecule consists of a single chain bound<br />

to the cell membrane by phosphatidylinositol. Paroxysmal<br />

nocturnal hemoglobulinuria develops as a consequence of<br />

DAF deficiency.<br />

decomplementation<br />

Deliberate inactivation of complement in vitro or in vivo. To<br />

decomplement serum to remove hemolytic action, the specimen<br />

may be heated to 56°C for 30 minutes. Other methods<br />

for inactivation of complement include the addition of cobra<br />

venom factor, zymosan, or other substances that take up complement<br />

from the medium in which they are placed. Removal<br />

of complement activity in living animals may be accomplished<br />

through the injection of cobra venom factor or other<br />

substances to use up or inactivate the complement system.<br />

decorating<br />

Term describing the reaction of tissue antigens with<br />

monoclonal antibodies, also known as staining in the<br />

immunoperoxidase reaction. Thus, a tissue antigen stained<br />

with a particular antibody is said to be decorated with that<br />

monoclonal antibody. Immunoperoxidase techniques give a<br />

reddish-brown color to the reaction product that is read by<br />

light microscopic observation.<br />

defective endogenous retroviruses<br />

Partial retroviral genomes that are integrated into host cell<br />

DNA and carried as host genes.<br />

defensins<br />

Widely reactive antimicrobial cationic proteins present<br />

in polymorphonuclear neutrophilic leukocyte granules.<br />

They block cell transport activities and are lethal for<br />

Gram-positive and Gram-negative microorganisms. These<br />

peptides are rich in cystesine and are found in the skin and<br />

in neutrophil granules that function as broad-spectrum antibiotics<br />

that kill numerous bacteria and fungi. The inflammatory<br />

cytokines, interleukin-1 (IL1) and tumor necrosis<br />

factor (TNF), facilitate synthesis of defensins. Defensins<br />

(human neutrophil proteins 1–4) are amphipathic, carbohydrate-free,<br />

cytotoxic, membrane-active antimicrobial<br />

molecules. Three of the defensin peptides (HP-1, HP-2,<br />

and HP-3) are nearly identical in sequence. By contrast, the<br />

sequences of HP-4, H-5, and HP-6 are very different. HP-1<br />

and HP-2 are chemotactic for monocytes. High concentrations<br />

of HP-1 to -4 (25 to 200 μg/mL) manifest antimicrobial<br />

and/or viricidal properties in vitro. HP-4 has the<br />

greatest defensin activity, and HP-3 the least.<br />

deficiency of secondary granules<br />

A rare disorder in which neutrophils are bereft of secondary<br />

granules, a condition that has an autosomal-recessive<br />

mode of inheritance. Affected individuals show increased<br />

incidence of infection by pyogenic microorganisms.<br />

degenerate binding specificity<br />

A form of antigen-binding specificity shown by major<br />

histocompatibility complex (MHC) class I and II molecules.<br />

Each MHC allotype may bind numerous peptides of different<br />

amino acid sequences.<br />

degranulation<br />

A mechanism whereby cytoplasmic granules in cells fuse<br />

with cell membranes to discharge the contents from the<br />

cells. A classic example is degranulation of mast cells or<br />

basophils in immediate (type I) hypersensitivity. In phagocytic<br />

cells, cytoplasmic granules combine with phagosomes<br />

and release their contents into the phagolysosome formed<br />

by their union. The contents of intracytoplasmic granules<br />

are released to the outsides of cells, rendering the granules<br />

no longer visible microscopically. The discharge may be<br />

into a phagosome as well as into the external environment.<br />

Degranulation is observed in selected cells that participate<br />

in inflammatory and immunological reactions.<br />

Macrophage<br />

Langerhans<br />

cell<br />

Antigen<br />

T lymphocyte<br />

Lymphatic<br />

Venule<br />

Delayed-type hypersensitivity.<br />

Lymphatic<br />

T lymphocyte

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