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schlepper 638 scratch test<br />

schlepper<br />

Landsteiner’s term for large macromolecules that serve as<br />

carriers for simple chemical molecules serving as haptens.<br />

The immunization of rabbits and other animals with a<br />

hapten–carrier complex leads to the formation of antibodies<br />

specific for the hapten and the carrier. T cells were later<br />

shown to be carrier-specific and B cells hapten-specific.<br />

Carriers are conjugated to haptens through covalent linkages<br />

such as the diazo linkage.<br />

Schultz–Dale test (historical)<br />

Strong contraction of the isolated uterine horn muscle<br />

of a virgin guinea pig that has been actively or passively<br />

sensitized occurs following the addition of specific antigen<br />

to a 37°C tissue bath in which it is suspended. This reaction<br />

is the basis for an in vitro assay of anaphylaxis termed the<br />

Schultz–Dale test. Muscle contraction is caused by the<br />

release of histamine and other pharmacological mediators<br />

of immediate hypersensitivity following antigen interaction<br />

with antibody fixed to tissue cells.<br />

SCID (severe combined immunodeficiency)<br />

Refer to severe combined immunodeficiency syndrome.<br />

SCID (severe combined immunodeficiency, human–mouse)<br />

A murine immunodeficiency in which human immune system<br />

elements such as bone marrow and thymic fragments<br />

have been introduced. Pluripotent human hematopoietic<br />

stem cells differentiate into mature immunocytes in these<br />

mice, rendering them useful for investigating lymphocyte<br />

development.<br />

SCID (severe combined immunodeficiency, mouse)<br />

An autosomal-recessive mutation expressed as severe<br />

combined immune deficiency in the CB-17Icr mouse<br />

strain. These mice do not have serum immunoglobulins,<br />

yet their adenosine deaminase (ADA) levels are normal.<br />

They lack T and B lymphocytes and thus fail to respond<br />

to T cell-dependent or -independent antigens when challenged.<br />

Likewise, their lymph nodes and spleen cells fail<br />

to proliferate following challenge by T or B lymphocyte<br />

mitogens. The lymphoid stroma in their lymph nodes and<br />

spleen is normal. Even though they exhibit no evidence of T<br />

cell-mediated immunity, they have natural killer (NK) cells<br />

and mononuclear phagocytes that are normal in number and<br />

function. The mutation likewise does not affect myeloid and<br />

erythroid lineage cells. B cell development is arrested at the<br />

pro-B stage before cytoplasmic or surface immunoglobulins<br />

are present. Normal numbers of macrophages are present<br />

in the spleen, peritoneum, and liver. The SCID mutation is<br />

associated with an intrinsic defect in lymphoid stem cells.<br />

The main characteristic of SCID mice is the failure of their<br />

lymphocytes to express antigen-specific receptors due to<br />

disordered rearrangements of T cell receptors or immunoglobulin<br />

genes. The defect in recombination of antigenspecific<br />

receptor genes may be associated with the absence<br />

of a DNA recombinase specific for lymphocytes in these<br />

mice. Attributable to a defect in DNA-PK function requisite<br />

for V(D)J recombination. This mouse model may be used<br />

to substitute for human experimentation to investigate the<br />

effects of anti-HIV drugs and immunostimulants. It is also<br />

useful for investigations of neoplasms in hosts lacking<br />

effective immune responses.<br />

Scl-70 antibody<br />

An antinuclear antibody found in as many as 70% of<br />

patients with diffuse-type scleroderma (progressive<br />

systemic sclerosis) who experience extensive and rapid skin<br />

involvement and early visceral manifestations.<br />

Scl-70 (topoisomerase I) autoantibodies.<br />

Scl-70 (topoisomerase I) autoantibodies<br />

Autoantibodies found in 20 to 40% of diffuse scleroderma<br />

patients. Two thirds of patients with these autoantibodies<br />

have diffuse scleroderma and 20% of patients with limited<br />

scleroderma manifest topoisomerase I autoantibodies. Sc1-70<br />

autoantibodies or DR3-DRw52a tissue types represent a<br />

17-fold increase in risk for development of pulmonary fibrosis<br />

in scleroderma. These autoantibodies are occasionally found<br />

in classical systemic lupus erythematosus (SLE) without<br />

manifestations of scleroderma. Topoisomerase I autoantibodies<br />

portend a poor prognosis in Raynaud’s phenomenon.<br />

Silica can induce a scleroderma-like condition. Some patients<br />

develop Scl-70 autoantibodies. The preferred technique for<br />

detection of IgG autoantibodies against topoisomerase I is<br />

enzyme immunoassay (EIA) with immunoblot confirmation.<br />

The relevance of an association of topoisomerase I autoantibodies<br />

with neoplasms remains to be determined.<br />

scleroderma<br />

Refer to progressive systemic sclerosis.<br />

SCM-1<br />

Single cysteine motif 1 (SCM-1) is a member of the γ (C)<br />

family of chemokines. cDNA clones derived from human<br />

peripheral blood mononuclear cells stimulated with phytohemagglutinin<br />

(PHA) encode SCM-1, which is significantly<br />

related to the α and β chemokines. It has only the second<br />

and fourth of four cysteines conserved in these proteins. It<br />

is 60.5% identical to lymphotactin. SCM-1 and lymphotactin<br />

are believed to represent human and mouse prototypes<br />

of a γ (C) chemokine family. SCM-1 is expressed by human<br />

T cells and spleen.<br />

sCR1 (soluble complement receptor type 1)<br />

A substance prepared by recombinant DNA technology that<br />

combines with activated C3b and C4. This facilitates their<br />

inactivation by complement factor I. sCR1 significantly<br />

diminishes myocardial injury induced by hypoxia in rats.<br />

scratch test<br />

Skin test for the detection of immunoglobulin E (IgE) antibodies<br />

against a particular allergen that are anchored to mast<br />

cells in the skin. After scratching the skin with a needle, a<br />

minute amount of aqueous allergen is applied to the scratch<br />

site, and the area is observed for the development of urticaria

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