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Untitled - D Ank Unlimited

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estitope 619 reticulin autoantibodies<br />

Resting lymphocyte<br />

12 µm<br />

Resting lymphocyte.<br />

Activated lymphocyte<br />

nucleus usually has a poorly visible single indentation and<br />

contains densely packed chromatin. Occasionally, nucleoli<br />

can be distinguished. The small lymphocyte variant—the<br />

predominant morphologic form—is slightly larger than an<br />

erythrocyte. Larger lymphocytes ranging from 10 to 20 μm<br />

in diameter are difficult to differentiate from monocytes.<br />

They have more cytoplasm and may show azurophilic<br />

granules. Intermediate-size forms are also described. Under<br />

phase contrast microscopy, living lymphocytes show feeble<br />

motility with amoeboid movements that give the cells<br />

hand-mirror shapes. The mirror handle is called a uropod.<br />

In large lymphocytes, mitochondria and lysosomes are<br />

better visualized, and some cells show spherical, birefringent,<br />

0.5-μm diameter inclusions called Gall bodies.<br />

Lymphocytes do not spread on surfaces. The different<br />

classes of lymphocytes cannot be distinguished by light<br />

microscopy. B lymphocytes sometimes show hairy (rough)<br />

surfaces under scanning electron microscopy (SEM), but<br />

thes are apparently artifacts. Electron microscopy does not<br />

provide additional information except for visualization of<br />

cellular organelles that are not abundant. This suggests that<br />

the small resting lymphocytes are end-stage cells; however,<br />

under appropriate stimulation, they are capable of considerable<br />

morphologic changes.<br />

restitope<br />

That segment of a T cell receptor that makes contact and<br />

interacts with a class II histocompatibility antigen molecule<br />

during antigen presentation.<br />

restriction endonucleases<br />

Bacterial products that identify and combine with a short<br />

sequence of DNA. The enzyme acts as molecular scissors<br />

by cleaving the DNA at the recognition site or at another<br />

location. Restriction endonucleases catalyze degradation<br />

of foreign DNA. They recognize precise base sequences<br />

of DNA and cut it into relatively few fragments, termed<br />

restriction fragments. The three major types of restriction<br />

endonucleases are (1) type I enzymes that identify specific<br />

base sequences but cut the DNA elsewhere (approximately<br />

1000 bp from the recognition site); (2) type II enzymes that<br />

identify specific base sequences and cut the DNA within or<br />

adjacent to these sequences; and (3) type III endonucleases<br />

that identify specific base sequences and cut the DNA<br />

approximately 25 bp from the recognition site.<br />

restriction fragment-length polymorphism (RFLP)<br />

Genome diversity in DNA from different subjects revealed<br />

by restriction map comparisons. This diversity is based<br />

on differences in restriction fragment lengths determined<br />

by sites of restriction endonuclease cleavage of the DNA<br />

molecules and revealed by preparing southern blots using<br />

appropriate molecular hybridization probes. Polymorphisms<br />

may be demonstrated in exons, introns, flanking sequences,<br />

or any DNA sequence. Variations in DNA sequence show<br />

Mendelian inheritance. Results are useful in linkage studies<br />

and can help to identify defective genes associated with<br />

inherited disease.<br />

restriction map<br />

A diagram of a linear or circular molecule of DNA<br />

that indicates the points where one or more restriction<br />

enzymes cleave the DNA. DNA is first digested with<br />

restriction endonucleases that split the DNA into fragments<br />

that can be separated by gel electrophoresis. Size<br />

determination is accomplished by comparison with fragments<br />

of known size.<br />

reticular cell<br />

Stroma or framework cells that, with reticular fibers, constitute<br />

the lymphoid tissue framework of lymph nodes, spleen,<br />

and bone marrow.<br />

reticular dysgenesis<br />

The most severe form of all combined immunodeficiency<br />

disorders. Leads to a failure in the development of B cells, T<br />

cells, NK cells, and granulocytes. This condition is incompatible<br />

with life and leads to early death of affected infants.<br />

The only possibility for treatment is hematopoietic stem cell<br />

transplantation or bone marrow transplantation. This condition<br />

has an autosomal-recessive mode of inheritance.<br />

reticulin antibodies<br />

Antibodies of five separate types of which the R 1 RA is of<br />

greatest interest. Immunoglobulin A (IgA) R 1 ARAs show<br />

more than 98% specificity for untreated celiac disease;<br />

however, sensitivity is only 20 to 25%.<br />

Reticulin autoantibodies.<br />

reticulin autoantibodies<br />

R 1 ARA is the only one of five separate reticulin autoantibodies<br />

that has diagnostic and pathogenic significance. IgA<br />

R 1 ARAs are highly specific for untreated celiac disease<br />

(CD). Approximately 2.6% of healthy children possess<br />

reticulin autoantibodies. In IgA-deficient subjects under<br />

evaluation for CD, the detection of IgG ARA, IgG gliadin<br />

autoantibodies (AGA), and IgG endomysial autoantibodies<br />

(EmAs) may be helpful. R 1 ARAs classically disappear 3 to<br />

12 months following the maintenance of a strict gluten-free<br />

diet in both adults and children with CD. IgA, ARA, IgA<br />

AGA, and IgA EmA may be detected in dermatitis herpetiformis<br />

(DH).<br />

R

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