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thymus-independent (TI) antigen 703 thyroiditis, autoimmune
thymus-independent (TI) antigen
An immunogen that can stimulate B cells to synthesize
antibodies without participation by T cells. These antigens
are less complex than thymus-dependent antigens. They
are often polysaccharides that contain repeating epitopes
or lipopolysaccharides (LPSs) derived from Gram-negative
microorganisms. Thymus-independent antigens induce
IgM synthesis by B lymphocytes without cooperation by
T cells. They do not stimulate immunological memory.
Humoral immune responses to T-independent antigens
show only minor heavy chain isotype switching or affinity
maturation, both of which require helper T cell signals. TI
antigens are classified as TI-1, which have intrinsic B cell
activating activity, or TI-2, which have multiple identical
epitopes that cross link B cell receptors. Murine TI antigens
are classified as TI-1 or TI-2. LPS, which activates murine
B cells without participation by T or other cells, is a typical
TI-1 antigen. Low LPS concentrations stimulate synthesis
of specific antigen; high concentrations activate growth
and differentiation of essentially all B cells. TI-2 antigens
include polysaccharides, glycolipids, and nucleic acids.
When T lymphocytes and macrophages are depleted, no
antibody response develops against them. Somatic hypermutation
and memory B cell development are lacking. The
antigens induce a low affinity primary IgM response. TI-1
antigens are usually large polymeric proteins that interact
with B cell receptors, leading to B cell activation without T
cell help. TI-2 antigens, usually polysaccharides composed
of repetitive elements, interact with B cell receptors but are
incapable of completely activating B cells without cytokines
provided by bystander cells.
thymus-replacing factor (TRF)
Interleukin-5 (IL5).
thyroglobulin
A thyroid protein demonstrable by immunoperoxidase
staining that serves as a marker for papillary and/or follicular
thyroid carcinomas.
thyroglobulin autoantibodies
Autoantibodies found in the sera of patients with such
thyroid disorders as chronic lymphocytic (Hashimoto’s)
thyroiditis (76 to 100%), primary myxedema (72%),
hyperthyroidism (33%), colloid goiter (7%), adenoma
(28%), thyroid cancer based on type (13 to 65%), pernicious
anemia (27%), autoimmune diseases, e,g., Addison’s
disease (28%), and diabetes mellitus (20%). Thyroglobulin
autoantibodies can be detected in normal subjects, diminishing
their clinical usefulness; 18% of women have these
antibodies that increase in frequency up to 30% as they
age. They are much less prevalent in men (approximately
3 to 6%), in whom they also increase with age. Enzyme
immunoassay (EIA), immunoradiometric assay (IRMA),
and chemiluminescence (CL) are the assays of choice for
these autoantibodies.
thyroid antibodies
Autoantibodies present in patients with Hashimoto’s
thyroiditis or thyrotoxicosis (Graves’ disease) that are
organ-specific for the thyroid. Antibodies against thyroglobulin
and autoantibodies against the microsomal antigen
of thyroid acinar cells may appear in patients with
autoimmune thyroiditis. Antibodies against thyroid-stimulating
hormone (TSH) receptors appear in patients with
Graves’ disease and cause stimulatory hypersensitivity.
Thyroid autoantibodies.
They mimic the action of TSH. They are IgG molecules
known as long-acting thyroid stimulator (LATS). LATS
levels are increased in many patients with thyrotoxicosis
or Graves’ disease.
thyroid autoantibodies
Autoantibodies found in patients with Hashimoto’s thyroiditis
or thyrotoxicosis (Graves’ disease) that are organspecific
for the thyroid. Antibodies against thyroglobulin
and autoantibodies against the microsomal antigen of
thyroid acinar cells may appear in patients with autoimmune
thyroiditis. Antibodies against TSH receptors appear
in Graves’ disease patients and cause stimulatory hypersensitivity.
They mimic the action of TSH. They are IgG
molecules known as long-acting thyroid stimulator (LATS).
LATS levels are increased in many patients with thyrotoxicosis
or Graves’ disease.
thyroid gland
Endocrine tissue encircling the trachea that synthesizes
and releases thyroxine, a hormone that regulates the rate
of metabolism.
thyroid autoimmunity animal models
Spontaneous and experimentally induced thyroiditis are the
two models used in research. Spontaneous models of thyroiditis
include OS chickens, BUF and BB rat strains, NOD
mice, and a special colony of beagle dogs. Genetic and
environmental factors contribute to autoimmune thyroid
disease. Genetic susceptibility to thyroid autoimmunity is
multifaceted and diverse. Major histocompatibility complex
(MHC) class II genes are the principal genetic determinants
of susceptibility in most species. Autoimmunity commences
as a response to a restricted region of the thyroglobulin
molecule, but a number of epitopes are present in that
region. Autoimmunity differs among species. Experimental
thyroiditis in mice is produced mainly by cytotoxic T cells;
antibodies play a significant pathogenetic role in spontaneous
thyroiditis of OS chickens.
thyroiditis, autoimmune
Hashimoto’s disease (chronic thyroiditis) is an inflammatory
disease found most frequently in middle-aged to older
women. Extensive lymphocyte infiltration of the thyroid
completely replaces the normal glandular structure of the
organ. The numerous plasma cells, macrophages, and germinal
centers give the appearance of node structure within
the thyroid. B cells and CD4 + T lymphocytes comprise
the principal infiltrating lymphocytes. Thyroid function is
first increased as the inflammatory reaction injures thyroid
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