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cartwheel nucleus 136 caspases<br />

Cartilaginous fishes.<br />

molecular weights are probably attributable to polymerization<br />

rather than differences in heavy chain class. The classic<br />

complement pathway components also make their debut.<br />

cartwheel nucleus<br />

The arrangement of chromatin in the nucleus of a typical<br />

plasma cell based on the more and less electron-dense areas<br />

observed by electron microscopy. Euchromatin makes up<br />

the less electron-dense spokes of the wheel, whereas heterochromatin<br />

makes up the more electron-dense areas.<br />

cascade reaction<br />

A sequential event in such enzymatic reactions as complement<br />

fixation and blood coagulation in which each stage of<br />

the reaction triggers the next appropriate step.<br />

caseation necrosis<br />

A type of necrosis present at the centers of large granulomas<br />

such as those formed in tuberculosis. The white cheesy appearance<br />

of the central necrotic area is the basis for the term.<br />

caseous necrosis<br />

Tissue destruction that occurs in tuberculosis and has the<br />

appearance of cottage cheese.<br />

M. tuberculosis<br />

Antigen<br />

presenting<br />

cell<br />

Caseous necrosis<br />

Class II<br />

MHC<br />

Bacillary<br />

antigenic<br />

peptide<br />

CD4<br />

Epithelioid cell<br />

T cell<br />

receptor<br />

CD4+<br />

T cell<br />

Delayed hypersensitivity<br />

Granuloma formation<br />

Giant cell<br />

Caseation necrosis.<br />

Casoni test<br />

A diagnostic skin test for hydatid disease in humans<br />

induced by Echinococcus granulosus infection. In sensitive<br />

individuals, a wheal and flare response develops within 30<br />

minutes following intradermal inoculation of a tapeworm or<br />

hydatid cyst fluid extract. This is followed within 24 hours<br />

by an area of induration produced by this cell-mediated,<br />

delayed-hypersensitivity reaction.<br />

caspase substrates<br />

The specificity of caspases translates into an order disassembly<br />

of cells by proteolytic cleavage of specific cellular<br />

protein. The paradigm substrate for caspase cleavage is<br />

PARP (polyADP-ribose polymerase). During apoptosis,<br />

intact 121-kDa PARP is cleaved by caspases into fragments<br />

of approximately 84 and 23 kDa. Generation of these<br />

fragments tends to be an inductor of apoptosis. Cleavage<br />

inactivates the enzymatic activity of PARP.<br />

caspases<br />

Closely related cysteine proteases that cleave protein substrates<br />

at the C terminal sides of aspartic acid residues and represent<br />

components of enzymatic cascades that lead to apoptotic cell<br />

death. There are two pathways of activation of caspases in<br />

lymphocyte. One involves mitochondrial permeability changes<br />

in growth factor-deprived cells, and the other involves signals<br />

from death receptors in plasma membranes. Cytosolic aspartate-specific<br />

proteases, called caspases, are responsible for the<br />

deliberate disassembly of cells into apoptotic bodies. Caspases<br />

are present as inactive proenzymes, most of which are activated<br />

by proteolytic cleavage. Caspase 8, caspase 9, and caspase 3 are<br />

situated at the pivotal junctions in apoptotic pathways. Caspase<br />

8 initiates disassembly in response to extracellular apoptosisinducing<br />

ligands and is activated in a complex associated<br />

Sensitized T cell<br />

Lymphocyte<br />

Fibroblast<br />

Cytokines<br />

Immunity<br />

Activated macrophage

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