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Untitled - D Ank Unlimited

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tuberculin hypersensitivity 719 tumor antigens<br />

tuberculin hypersensitivity<br />

A form of bacterial allergy specific for a product in culture<br />

filtrates of Mycobacterium tuberculosis which, when<br />

injected into the skin, elicits a cell-mediated delayedtype<br />

(type IV) hypersensitivity response. Tuberculin-type<br />

hypersensitivity is mediated by CD4 + T lymphocytes. After<br />

intracutaneous inoculation of tuberculin extract or purified<br />

protein derivative (PPD), an area of redness and induration<br />

develops at the site in 24 to 48 hours in individuals subjected<br />

to present or past interaction with M. tuberculosis.<br />

tuberculin reaction<br />

A test of in vivo cell-mediated immunity. Robert Koch<br />

observed localized skin lesions of tuberculous guinea pigs<br />

inoculated intradermally with broth from a culture of tubercle<br />

bacilli. The body’s immune response to infection with<br />

the tubercle bacillus is signaled by the appearance of agglutinins,<br />

precipitins, opsonins, and complement-fixing antibodies<br />

in the serum. This humoral response is, however, not<br />

marked, and such antibodies are present in low titer. The<br />

most striking response is the development of delayed-type<br />

hypersensitivity (DTH) that plays a protective role in preventing<br />

reinfection with the same organism. Subcutaneous<br />

inoculation of tubercle bacilli in a normal animal produces<br />

no immediate response, but in 10 to 14 days a<br />

nodule develops at the site of inoculation. The nodule then<br />

becomes a typical tuberculous ulcer. The regional lymph<br />

nodes become swollen and caseous. In contrast, a similar<br />

inoculation in a tuberculous animal induces an indurated<br />

area at the site of injection within 1 to 2 days. This becomes<br />

a shallow ulcer that heals promptly. No swelling of the<br />

adjacent lymphatics is noted. The tubercle bacillus antigen<br />

responsible for DTH is wax D, a lipopolysaccharide–protein<br />

complex of bacterial cell walls. The active peptide consists<br />

of diaminopimelic acid, glutamic acid, and alanine. Testing<br />

for DTH to the tubercle bacillus is done with tuberculin,<br />

a heat-inactivated culture extract containing a mixture of<br />

bacterial proteins, or with PPD, a purified protein derivative<br />

of culture in nonproteinaceous media. Each compound<br />

alone is capable of sensitizing the recipient. The protective<br />

role of DTH is supported by the observation that in positive<br />

reactors living cells are usually free of tubercle bacilli and<br />

the bacteria are present in necrotic areas, separated by an<br />

avascular barrier. By contrast, in infected individuals producing<br />

negative reactions, the tubercle bacilli are found in<br />

great numbers in living tissues. The reaction is permanently<br />

or transiently negative in individuals whose cell-mediated<br />

immune responses are transiently or permanently impaired.<br />

tuberculin test<br />

The 24- to 48-hour response to intradermal injection of<br />

tuberculin. If positive, it signifies delayed-type (type IV)<br />

hypersensitivity to tuberculin and implies cell-mediated<br />

immunity to Mycobacterium tuberculosis. The intradermal<br />

inoculation of tuberculin or purified protein derivative<br />

(PPD) produces an area of erythema and induration within<br />

24 to 48 hours in positive individuals. A positive reaction<br />

signifies the presence of cell-mediated immunity to M.<br />

tuberculosis as a consequence of past or current exposure to<br />

the microorganism; however, tuberculin is not a test for the<br />

diagnosis of active tuberculosis.<br />

tuberculin-type reaction<br />

A cell-mediated delayed-type hypersensitivity skin response<br />

to an extract such as candidin, brucellin, or histoplasmin.<br />

Individuals who experience positive reactions have delayedtype<br />

hypersensitivity or cell-mediated immunity mediated<br />

by T lymphocytes following contact with the microorganism<br />

in question.<br />

tuberculosis immunization<br />

The induction of protective immunity through injection of<br />

an attenuated vaccine containing bacille Calmette-Guérin<br />

(BCG). This vaccine was more widely used in Europe<br />

than in the United States in attempts to provide protection<br />

against tuberculosis. A local papule develops several weeks<br />

after injection in individuals who were previously tuberculin-negative.<br />

The vaccine is not administered to positive<br />

individuals. The vaccine is claimed to protect against development<br />

of tuberculosis, although not all authorities agree<br />

on its efficacy for this purpose. In recent years, oncologists<br />

have used BCG vaccine to reactivate the cellular immune<br />

systems of patients bearing neoplasms in the hope of facilitating<br />

antitumor immunity.<br />

tubular basement membrane autoantibodies<br />

Autoantibodies specific for tubular basement membranes<br />

(TBMs). They are detectable by immunofluorescence in<br />

some renal allotransplant patients following certain types<br />

of drug therapy and occasionally without a known cause. In<br />

human tubulointerstitial nephritis (TIN), TBM autoantibodies<br />

generated react with a major 58-kDa antigen (TIN antigen)<br />

and minor 160-, 175-, and 300-kDa antigens related<br />

to laminin and entactin/nidogen. Twenty-two percent of<br />

patients with various types of interstitial nephritis manifest<br />

autoantibodies against TIN antigen. Normal urine may<br />

reveal human TBM antigens that are capable of inducing<br />

TIN in rats. TBM autoantibodies are only rarely detected<br />

in human cases of TIN, but they are often prominent as<br />

glomerular basement membrane (GBM) autoantibodies in<br />

patients with Goodpasture’s syndrome. TBM autoantibodies<br />

are of unknown clinical significance.<br />

tuftsin<br />

A leukokinin globulin-derived substance that enhances<br />

phagocytosis. It is a tetrapeptide comprised of Thr–Lys–<br />

Pro–Arg. The leukokinin globulin from which it is derived<br />

represents immunoglobulin Fc receptor residues 289<br />

through 292. Tuftsin is formed in the spleen. Its actions<br />

include neutrophil and macrophage chemotaxis, enhancing<br />

phagocyte motility, and promoting oxidative metabolism. It<br />

also facilitates antigen processing.<br />

tuftsin deficiency<br />

A tetrapeptide that stimulates phagocytes. Tuftsin is split<br />

from an immunoglobulin by the action of one proteolytic<br />

enzyme in the spleen that cleaves the carboxyl terminus<br />

between residues 292 and 293 and another enzyme<br />

(leukokinase) confined to neutrophil membranes that splits<br />

the molecule between positions 288 and 289. Thus, tuftsin<br />

deficiency, which is transmitted as an autosomal-recessive<br />

trait, results from a lack of this splenic enzyme. Although γ<br />

globulin has been used, there is no known treatment.<br />

tumor<br />

A neoplasm developing as a consequence of uncontrolled<br />

cell proliferation. Benign tumors are self-limiting, whereas<br />

malignant tumors may be invasive.<br />

tumor antigens<br />

Cell surface proteins on tumor cells that can induce a cellmediated<br />

and/or humoral immune response. Refer also to<br />

tumor-associated antigens and tumor-specific antigens.<br />

T

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