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thyrotoxicosis 704 tissue-specific antigen<br />

follicles, causing them to release thyroid hormones.<br />

This stage is soon replaced by hypothyroidism in the<br />

later stages of Hashimoto’s thyroiditis. Patients with this<br />

disease have enlarged thyroid glands. Circulating autoantibodies<br />

against thyroglobulin and thyroid microsomal<br />

antigen (thyroid peroxidase) are present. Cellular sensitization<br />

to thyroid antigens may also be detected. Thyroid<br />

hormone replacement therapy is given for the hypothyroidism<br />

that develops.<br />

thyrotoxicosis<br />

Disease of the thyroid characterized by hyperthyroidism<br />

with elevated levels of thyroid hormones in the blood and<br />

thyroid gland hyperplasia or hypertrophy. Thyrotoxicosis<br />

may be autoimmune, as in Graves’ disease, in which diffuse<br />

goiter may be observed. Autoantibodies specific for thyroid<br />

antigens mimic thyroid-stimulating hormones (TSHs) by<br />

stimulating thyroid cell function. In addition, patients with<br />

Graves’ disease develop ophthalmopathy and proliferative<br />

dermopathy. The disease occurs predominantly in females<br />

(70 females to 1 male) and usually appears in the 30- to<br />

40-year old age group. In Caucasians, it is a disease associated<br />

with DR3. Patients may develop nervousness, tachycardia,<br />

and other symptoms of hyperthyroidism. They also<br />

have increased levels of total and free T3 and T4 along with<br />

a diffuse and homogeneous uptake of radioactive iodine.<br />

Three types of antithyroid antibodies occur: (1) thyroidstimulating<br />

immunoglobulin, (2) thyroid growth-stimulating<br />

immunoglobulin, and (3) thyroid binding-inhibitory<br />

immunoglobulin. Their presence confirms a diagnosis<br />

of Graves’ disease. The thyroid gland may be infiltrated<br />

with lymphocytes. Long-acting thyroid stimulator (LATS)<br />

is classically associated with thyrotoxicosis. It is an IgG<br />

antibody specific for thyroid hormone receptors. It induces<br />

hyperactivity by combining with TSH receptors.<br />

thyrotropin<br />

Thyroid-stimulating hormone (TSH).<br />

thyrotropin receptor autoantibodies<br />

Autoantibodies specific for thyrotopin receptor (TSHR) are<br />

very heterogeneous. Some TSHR antibodies stimulate the<br />

receptor and are associated with Graves’ disease (hyperthyroidism).<br />

Others are inhibitory. Thyrotopin-binding inhibitory<br />

immunoglobulin (TBII) antibodies bind to TSHR and<br />

inhibit binding of TSH to receptors. Thyroid-stimulating<br />

antibodies (TSAbs) mimic TSH and induce thyroid cells to<br />

increase cAMP production in a bioassay. Long-acting thyroid<br />

stimulator (LATS), a growth-promoting immunoglobulin<br />

(IgG) found in Graves’ disease, interacts with TSHR.<br />

TSHR antibodies are measured by receptor assays. TS<br />

antibodies are 95% in Graves’ disease and correlate closely<br />

with disease activity. TSB antibodies are associated closely<br />

with atrophic gastritis and severe hypothyroidism, yet atrophic<br />

thyroiditis may occur in their absence. TBII and TS<br />

Bantibodies occur in nongoiterous autoimmune thyroiditis.<br />

Placental passage of TSHR antibodies may induce transient<br />

hypo- or hyperthyroidism.<br />

thyroxine<br />

A hormone synthesized and released by the thyroid gland<br />

that regulates cell metabolism, body temperature, use of<br />

energy, and normal functioning of the central nervous and<br />

cardiovascular systems.<br />

TI antigen<br />

Abbreviation for T-independent (Td) antigen.<br />

TI-1 antigen, TI-2 antigen<br />

Refer to thymus-independent antigen.<br />

tight junction<br />

Juncture between the apical poles of epithelial cells that<br />

blocks the passive diffusion of pathogenic microorganisms,<br />

macromolecules, and peptides but can be unblocked by<br />

cytokine signaling.<br />

tight skin 1 (Tsk1) mouse<br />

A mouse strain developed from a spontaneous dominant<br />

mutation in the inbred B10.D2(58N)/Sn strain that represents<br />

a genetically transmitted model of systemic sclerosis.<br />

The effects of the Tsk1 mutation include excessive accumulation<br />

of collagen in the dermis and various internal organs,<br />

thereby mimicking major aspects of human systemic<br />

sclerosis. The principal visceral changes in Tsk1/+ occur in<br />

the lungs and heart. Lungs are greatly distended and histologically<br />

resemble human emphysema with little fibrosis.<br />

Alveolar spaces are markedly dilated with thin disrupted<br />

walls and subpleural cysts and bullae. Myocardial hypertrophy<br />

with increased collagen deposition is present.<br />

tight skin 2 (Tsk2) mouse<br />

A mouse strain with features resembling those of both<br />

human systemic sclerosis and the original tight skin mutation<br />

of the mouse, Tsk1.<br />

TIL<br />

Abbreviation for tumor-infiltrating lymphocyte.<br />

tine test<br />

A human tuberculin test involving intradermal inoculation<br />

of dried, old tuberculin using a four-pointed applicator that<br />

introduces the test substance 2 mm below the surface.<br />

tingible body<br />

Nuclear debris present in macrophages of lymph node,<br />

spleen, tonsil germinal centers, and the dome of the appendix.<br />

tingible body macrophages<br />

Phagocytic cells that engulf apoptotic B cells. They form in<br />

large numbers at the height of a germinal center response.<br />

TIR domain<br />

Toll/IL-1R domain present in Toll-like receptor cytoplasmic<br />

tails, IL1R, and selected plant pattern recognition molecules.<br />

Possesses no intrinsic tyrosine kinase activity but<br />

acquires the MyD88 adaptor protein.<br />

Tiselius, Arne W. K. (1902–1971)<br />

Swedish chemist educated at the University of Uppsala,<br />

where he also conducted research. In 1934, he was at the<br />

Institute for Advanced Study in Princeton, and in 1946 he<br />

worked for the Swedish National Research Council. He was<br />

awarded the Nobel Prize in Chemistry in 1948 and became<br />

president of the Nobel Foundation in 1960. With Elvin A.<br />

Kabat, he perfected the electrophoresis technique and classified<br />

antibodies as γ globulins. He also developed synthetic<br />

blood plasmas.<br />

tissue-fixed macrophage<br />

Histiocyte.<br />

tissue-specific antigen<br />

An antigen restricted to cells of one type of tissue. Tissuespecific<br />

or organ-specific autoantibodies occur in certain<br />

types of autoimmune diseases. Organ-specific or tissuespecific<br />

antibodies are often not species-specific. For<br />

example, autoantibodies against human thyroglobulin may<br />

cross react with the corresponding molecules of other species.<br />

The antigen may be a protein or carbohydrate epitope<br />

present only in a particular tissue or subcellular site. When

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