26.07.2013 Views

Untitled - D Ank Unlimited

Untitled - D Ank Unlimited

Untitled - D Ank Unlimited

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

allotypic determinant 33 alternative complement pathway<br />

may also occur after administration of antibodies specific<br />

for the paternal allotype to heterozygous newborn rabbits.<br />

Animals conditioned in this way remain deficient for the<br />

suppressed allotype for months and possibly years thereafter.<br />

The animal switches to a compensatory increase in the<br />

production of the nonsuppressed allotype. In homozygotes,<br />

suppression involves heavy-chain switching from one Ig<br />

class to another.<br />

allotypic determinant<br />

Epitope on serum immunoglobulin (Ig) molecules present<br />

in selected members of a species. Allotypic determinants<br />

are present in addition to other markers characteristic of the<br />

molecule as a whole for the respective species. The allotypic<br />

determinants or allotopes are characteristic of a given class<br />

and subclass of immunoglobulin and have been demonstrated<br />

in several species. The inheritance of genes controlling these<br />

determinants is strictly Mendelian and is not sex linked. Both<br />

H and k L chains contain such determinants; the encoding<br />

genes are not linked and are codominant in an individual.<br />

This means that markers present both in the father and mother<br />

are expressed phenotypically in a heterozygote. However, an<br />

individual immunoglobulin-producing cell expresses only one<br />

of a pair of allelic genes, as a single cell can utilize only one<br />

parental chromosome. In an individual, some cells use the<br />

information encoded on the chromosome derived paternally<br />

and other cells use that derived from the maternal contribution.<br />

Thus, the individual is heterozygous, but a single cell secretes<br />

only the products of one allele because of allelic exclusion. The<br />

allotypic markers of human IgG are designated Gm determinants.<br />

The Km(Inv) markers are characteristic for the C region<br />

of k light chains.<br />

allotypic marker<br />

Refer to allotypic determinant or allotope.<br />

allotypic specificities<br />

Genetically different antibody classes and subclasses<br />

produced within individuals of the same species. They are<br />

detected as changes in the amino acid residues present in<br />

specific positions in various polypeptide chains. The allotypic<br />

specificities are also called genetic markers. Gm and Km(Inv)<br />

markers are examples of allotypes of human immunoglobulin<br />

G (IgG) heavy chains and k light chains, respectively.<br />

Alopecia areata.<br />

allotypy<br />

A term that describes the various allelic types or allotypes<br />

of immunoglobulin molecules.<br />

alopecia areata<br />

A partial or patchy loss of hair from the scalp or other<br />

hair site that is believed to have an autoimmune basis,<br />

even though no autoantigenic molecules in hair follicles<br />

have been identified. The inheritance is polygenic with<br />

a contribution from major histocompatibility complex<br />

(MHC) genes. Other autoimmune diseases associated<br />

with alopecia areata include the thyrogastric group,<br />

pernicious anemia, Addison’s disease, and diabetes, as<br />

well as vitiligo, systemic lupus erythematosus (SLE),<br />

and others. There is supportive serological evidence for<br />

autoimmunity in alopecia areata. Organ-specific autoantibodies<br />

are increased in frequency, especially to thyroid<br />

micosomal antigen and to other tissue antigens as well.<br />

Affected hair follicles are encircled by dense lymphocytic<br />

infiltrates that consist of T cells with CD8 + T cell subset<br />

predominance.<br />

alpha–beta T cells<br />

T lymphocytes that express an αβ TCR. They comprise<br />

Th, Tc, and regulatory T cell populations and mediate very<br />

specific and broadly diverse adaptive immune responses.<br />

ALPS<br />

Abbreviation for autoimmune lymphoproliferative<br />

syndromes.<br />

ALS (antilymphocyte serum) or ALG (anti-lymphocyte<br />

globulin)<br />

Refer to antilymphocyte serum.<br />

altered peptide ligand (APL)<br />

Analog of immunogenic peptide in which the T cell receptor<br />

contact sites have been altered, usually by substitution<br />

with another amino acid. Even though these peptides fail<br />

to stimulate T cell proliferation, they activate some T cell<br />

receptor-mediated functions. Antagonist peptides specifically<br />

downmodulate the agonist-induced response. APLs<br />

can act therapeutically by modulating the cytokine patterns<br />

of T cells or they may induce a form of anergy in T cells.<br />

They stimulate partial responses from T lymphocytes specific<br />

for the agonist peptide.<br />

altered self<br />

The concept that the linkage of non-self peptide to major<br />

histocompatibility complex (MHC) yields a peptide–MHC<br />

structure different from any found in normal cells of the<br />

individual.<br />

Alternaria species<br />

Aeroallergenic fungi that can induce hypersensitivity<br />

pneumonitis (HP). These fungi cause a form of HP known<br />

as woodworker’s lung disease, as well as immunoglobulin E<br />

(IgE)-mediated allergic disease.<br />

alternative C5 convertase<br />

A participant in the alternative pathway of complement<br />

activation, comprised of two C3b molecules linked to Β<br />

(C3b 2Bb) and splits C5 into C5a and C5b.<br />

alternative complement pathway<br />

Activation of complement not by antibody but through<br />

the binding of complement protein C3b to the surface<br />

of a pathogenic microorganism. This innate immune<br />

mechanism amplifies complement activation through the<br />

classic pathway. A non-antibody-dependent pathway for<br />

A

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!