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acetaldehyde adduct autoantibodies 6 acquired immune deficiency syndrome (AIDS)<br />

Gal<br />

α1 2<br />

Fuc<br />

β1 4<br />

GlcNAc<br />

β1 3<br />

Gal<br />

Gal = Galactose<br />

GlcNAc = N-acetylglucosamine<br />

Fuc = Fucose<br />

Chemical structure of H antigen which is a specificity of the ABO blood<br />

group system.<br />

CH 4<br />

CH 3<br />

RBC<br />

RBC<br />

H L<br />

IgM<br />

J chain<br />

VL<br />

CL<br />

RBC<br />

RBC<br />

CH 2<br />

CH 1<br />

Agglutination of human red blood cells (RBCs) by natural isohemagglutinins<br />

that are antibodies of the IgM class.<br />

Abrin-A<br />

Abrin.<br />

VH<br />

include the CD4 and CD8 coreceptors, CD3 components of<br />

the T cell receptor, adhesion molecules, and costimulatory<br />

molecules.<br />

acetaldehyde adduct autoantibodies<br />

Antibodies found in approximately 73% of alcoholic<br />

and in 39% of nonalcoholic liver disease (e.g., primary<br />

biliary cirrhosis, chronic active hepatitis, acute viral and<br />

drug-induced hepatitis). The highest titers of these autoantibodies<br />

are found in advanced stages of alcoholic and<br />

nonalcoholic liver disease. Alcoholics develop acetaldehyde<br />

adduct autoantibodies to apo B-containing lipoproteins,<br />

particularly very low density lipoproteins (VLDLs); 33%<br />

of alcoholic patients with heart muscle disease develop<br />

cardiac–protein–acetaldehyde adduct autoantibodies that<br />

could be potential markers for this heart condition.<br />

acetylcholine receptor (AChR) antibodies<br />

IgG autoantibodies that cause loss of function of AChRs<br />

that are critical to chemical transmission of the nerve<br />

impulse at the neuromuscular junction. This represents a<br />

type II mechanism of hypersensitivity, according to the<br />

Coombs and Gell classification. AChR antibodies are<br />

heterogeneous, with some showing specificity for antigenic<br />

determinants other than those that serve as acetylcholine<br />

or α-bungarotoxin binding sites. As many as 85 to 95% of<br />

myasthenia gravis patients may manifest AChR antibodies.<br />

acetylcholine receptor (AChR) autoantibodies<br />

Autoantibodies binding acetylcholine receptors react with<br />

several epitopes other than the binding site for ACh or<br />

α-bungarotoxin. They are found in 88% of patients with<br />

generalized myasthenia gravis (MG), 70% of patients<br />

with ocular myasthenia, and 80% of patients with MG<br />

in remission. They decrease in titer when weakness is<br />

reduced with immunosuppressive therapy. AChR-blocking<br />

autoantibodies react with the AChR binding site. They are<br />

found in 50% of patients with MG, in 30% of patients with<br />

ocular MG, and in 20% of patients with MG in remission.<br />

AChR-modulating autoantibodies crosslink AChRs and<br />

induce their removal from muscle membrane surfaces. They<br />

are present in more than 90% of patients with MG. AChR<br />

autoantibodies of one or more types are present in at least<br />

80% of patients with ocular MG.<br />

acoelomate<br />

A lower invertebrate animal lacking a body cavity.<br />

acquired agammaglobulinemia<br />

Refer to common variable immunodeficiency.<br />

acquired B antigen<br />

The alteration of A1 erythrocyte membrane through the<br />

action of such bacteria as Escherichia coli, Clostridium<br />

tertium, and Bacteroides fragilis to make it react as if it<br />

were a group B antigen. The named microorganisms can be<br />

associated with gastrointestinal infection or carcinoma.<br />

acquired C1 inhibitor deficiency<br />

A condition in which the C1 inhibitor is inactivated,<br />

resulting in elevated C4 and C2 cleavage as C1 is activated.<br />

Patients experience repeated laryngeal, intestinal,<br />

and subcutaneous tissue swelling. A kinin-like peptide<br />

derived from C2b promotes vascular permeability and<br />

produces symptoms. Subjects with B lymphocyte or plasma<br />

cell monoclonal proliferation may develop acquired C1<br />

inhibitor deficiency. These syndromes include multiple<br />

myeloma, Waldenström’s macroglobulinemia, and B cell<br />

lymphoma. Subjects may develop antiidiotypic antibodies<br />

against membrane immunoglobulins or myeloma proteins.<br />

Idiotype–anti-idiotype interactions at cell membranes may<br />

result in C1 fixation and may increase utilization of C4 and<br />

C2 as well as C1 inhibitor.<br />

acquired immune deficiency syndrome (AIDS)<br />

A retroviral disease marked by profound immunosuppression<br />

that leads to opportunistic infections, secondary<br />

neoplasms, and neurologic manifestations. It is caused by<br />

the human immunodeficiency virus 1 (HIV-1), the causative<br />

agent for most cases worldwide, with a few cases in western

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