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anaplastic 41 anergy
anaphylaxis (SRS-A), bradykinin, and platelet-activating factor.
In addition to systemic anaphylaxis described above, local anaphylaxis
may occur in the skin, gut, or nasal mucosa following
contact with the antigen. The skin reaction, called urticaria,
consists of a raised wheal surrounded by an area of erythema.
Cytotoxic anaphylaxis follows the interaction of antibodies
with cell surface antigens. See also aggregate anaphylaxis.
anaplastic
Tumor cells that are poorly differentiated and capable of
aggressive growth.
anatoxin
Antibody specific for exotoxins produced by certain
microorganisms such as the causative agents of diphtheria
and tetanus. Prior to the antibiotic era, antitoxins were the
treatments of choice for diseases produced by the soluble
toxic products of microorganisms, such as those from
Corynebacterium diphtheriae and Clostridium tetani.
anavenom
A toxoid consisting of formalin-treated snake venom that
destroys the toxicity but preserves the immunogenicity of
the preparation.
ancestral haplotype
An MHC haplotype that numerous families share, indicating
that they probably have common ancestors. Also called
HLA supratype or common extended haplotype.
anchor residues
Amino acid side chains of the peptide whose side chains fit
into pockets in the peptide-binding cleft of the major histocompatibility
complex (MHC) molecule. The side chains
anchor the peptide in the cleft of the MHC molecule by binding
two complementary amino acids in the MHC molecule.
anemia, drug-induced immune hemolytic
Acquired hemolytic anemia that develops as a consequence
of immunological reactions following the administration of
certain drugs. Clinically, this anemia resembles autoimmune
hemolytic anemia of idiopathic origin. A particular
drug may induce hemolysis in one patient, thrombocytopenia
in another, neutropenia in yet another patient, and
occasionally combinations of these in a single patient.
The drug-induced antibodies that produce these immune
cytopenias are cell-specific. Drugs that cause hemolysis by
complement-mediated lysis include quinine, quinidine, and
rifampicin, as well as chlorpropamide, hydrochlorothiazide,
IgE
Resting
Serine esterase inhibitor
Serine esterase
Antigen bound by IgE
Release of pharmacological
mediators of Type I
hypersensitivity
Comparison of resting basophil and mast cell in which serine esterase activity is blocked by serine esterase inhibitor with a mast cell or basophil undergoing
degranulation as a consequence of antigen interaction with Fab regions of cell surface IgE molecules in which the serine esterase inhibitor activity is removed.
Antigen
nomifensine phenacetin, salicylazosulfapyridine, the
sodium salt of p-aminosalicylic acid, and stibophen. Drugdependent
immune hemolytic anemia in which the mechanism
is extravascular hemolysis may occur with prolonged
high dose penicillin therapy or other penicillin derivatives
as well as cephalosporins and tetracycline.
anergic B cell
Lymphocyte anergy, also termed clonal anergy, is the failure
of B cell (or T cell) clones to react against antigen and may
represent a mechanism to maintain immunologic tolerance to
self. Anergic B cells express immunoglobulin D (IgD) at levels
equal to that of normal B cells but they downregulate IgM 5- to
50-fold. This downregulation is associated with an inhibition
in signaling, resulting in diminished phosphorylation of critical
signal transduction molecules associated with surface immunoglobulin.
Receptor stimulation of anergic B cells fails to release
intracellular calcium, a critical step in B cell activation. Anergic
B cells are unable to respond to subsequent exposure to cognate
antigen. Anergy may be a means whereby the immune system
silences potentially harmful B cell clones while permitting B
cells to live long enough to be exported to peripheral lymphoid
organs where anergic B cells may encounter a foreign antigen
to which they have a higher affinity than their affinity for self
antigen. If this were so, anergic B cells would be activated and
contribute to a protective immune response.
anergize
Inducing anergy in a cell.
anergized
The consequence of rendering a subject anergic.
anergy
Diminished or absent delayed-type hypersensitivity (i.e., type
IV hypersensitivity) as revealed by lack of responsiveness to
commonly used skin test antigens including PPD, histoplasmin,
candidin, etc. Decreased skin test reactivity may
be associated with uncontrolled infection, tumor, Hodgkin
disease, sarcoidosis, etc. There is decreased capacity of
T lymphocytes to secrete lymphokines when their T cell
receptors interact with a specific antigen. Anergy describes
nonresponsiveness to antigen. Individuals are anergic when
they cannot develop a delayed-type hypersensitivity reaction
following challenge with an antigen. T and B lymphocytes
are anergic when they cannot respond to their specific antigens.
Often associated with lack of costimulation.
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