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Untitled - D Ank Unlimited

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chief cell autoantibodies 166 cholera toxin<br />

chief cell autoantibodies<br />

Antibodies reactive with chief cells that are principal<br />

sources of PG1 (the main form of serum pepsinogen). They<br />

are significantly diminished in atrophic gastritis type A,<br />

which is associated with pernicious anemia. Autoantibodies<br />

against pepsinogen, a 41-Kda antigen, are more frequent<br />

in pernicious anemia than are intrinsic factor antibodies.<br />

Pepsinogen autoantibodies are also present in approximately<br />

50% of active duodenal ulcer patients, a quarter of<br />

whom may have autoantibodies against H + /K + ATPase.<br />

Chimera.<br />

chimera<br />

The presence in an individual of cells of more than one<br />

genotype. This can occur rarely under natural circumstances<br />

in dizygotic twins (such as in cattle) that share a<br />

placenta in which the blood circulation has become fused,<br />

causing the blood cells of each twin to circulate in the<br />

other. More commonly, it refers to a human or other animal<br />

that received a bone marrow transplant that provides a cell<br />

population consisting of donor and self cells. Tetraparental<br />

chimeras can be produced by experimental manipulation.<br />

The name chimera derives from a monster of Greek mythology<br />

that had the body of a goat, the head of a lion, and the<br />

tail of a serpent.<br />

chimeric antibodies<br />

Antibodies that have, for example, mouse Fv fragments for<br />

the Ag-binding portion of the molecule but Fc regions of<br />

human immunoglobulin (Ig) that convey effector functions.<br />

chimeric protein<br />

A molecular structure comprised of segments of at least<br />

two, or possibly more, different proteins.<br />

chimerism<br />

The presence of two genetically different cell populations<br />

within an animal at the same time.<br />

Chlamydia immunity<br />

Chlamydiae infect many animal species and various<br />

anatomical sites. No single pattern of host response can<br />

be described, but similarities in effector mechanisms may<br />

exist. The strain or serovar of the infecting microorganism<br />

is also significant. In vitro studies and genital respiratory<br />

and ocular animal models have provided most of the<br />

information about both protective and pathologic host<br />

responses. Acute inflammation is the initial response, with<br />

participation by polymorphonuclear leukocytes (PMNs)<br />

that may counteract the microorganisms but also cause<br />

pathologic changes. When chlamydiae infect epithelial<br />

cells, interleukin- (IL1) is released, as well as IL8, a potent<br />

PMN chemoattractant. When these microorganisms<br />

infect macrophages, lipopolysaccharide (LPS) triggers the<br />

synthesis of TNFα, IL1, and IL6. They may also activate<br />

the alternative pathway of complement. IL8, TNFα, and<br />

complement may induce chemotaxis of PMNs to the local<br />

site. ICAM-1, VCAM-1, and MAdCAM-1 are all detectable<br />

early in the infection and may be addressins responsible for<br />

PMN extravasation at sites of infection. Natural killer (NK)<br />

cells may appear early after infection of the genital tract.<br />

Chlamydial infection produces both humoral and cell-mediated<br />

immune responses. Cell-mediated immunity has been<br />

found important in both mouse and guinea pig models. The<br />

CD4 + T cells are the main subset responsible for protective<br />

cell-mediated immunity. In genital infections, the T H1<br />

subset of CD4 T cells is the principal cell type leading to<br />

the formation of high levels of IFN-γ, which is believed to<br />

have a protective role. In some models, antibody appears to<br />

be important in the resolution of infection. Antibody may<br />

neutralize chlamydial elementary bodies in vitro. Immunity<br />

to chlamydial infections is short lived. No effective vaccine<br />

for chlamydia infections in humans currently exists, but a<br />

veterinary vaccine is available.<br />

HOOC CH2 CH2 CH2 N<br />

CH 2 CH 2 Cl<br />

CH2 CH2 Cl<br />

Structure of chlorambucil (4-[bis (2-chloroethyl)] amino-phenylbutyric<br />

acid).<br />

chlorambucil (4-[bis(2-chloroethyl)]amino-phenylbutyric acid)<br />

An alkylating and cytotoxic drug. Chlorambucil is not as<br />

toxic as is cyclophosphamide and has served as an effective<br />

therapy for selected immunological diseases such as<br />

rheumatoid arthritis, systemic lupus erythematosus (SLE),<br />

Wegener’s granulomatosis, essential cryoglobulinemia, and<br />

cold agglutinin hemolytic anemia. Although it produces<br />

bone marrow suppression, it has not produced hemorrhagic<br />

cystitis and is less irritating to the gastrointestinal tract<br />

than cyclophosphamide. Chlorambucil increases the likelihood<br />

of opportunistic infections and the incidence of some<br />

tumors.<br />

chlorodinitrobenzene (1-chlor-2,4-dinitrobenzene)<br />

More often termed dinitrochlorobenzene (DNCB). A<br />

chemical substance used to test for a patient’s ability to<br />

develop the type of delayed-type hypersensitivity referred to<br />

as contact hypersensitivity. This is a type IV hypersensitivity<br />

reaction. The chemical is applied to a patient’s forearm.<br />

Following sufficient time for sensitization to develop, the<br />

patient’s other forearm is exposed to a second (test) dose of<br />

the same chemical. In an individual with an intact cellmediated<br />

limb of the immune response, a positive reaction<br />

develops at the second challenge site within 48 to 72 hours.<br />

Individuals with cell-mediated immune deficiency disorders<br />

fail to develop a positive delayed-type hypersensitivity<br />

reaction.<br />

cholera toxin<br />

A Vibro cholerae enterotoxin comprised of five B subunits<br />

that are cell-binding, 11.6-kDa structures that encircle a<br />

27-kDa catalase that conveys ADP-ribose to G protein,<br />

leading to continual adenyl cyclase activation. Other toxins

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