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T h1 cells 693 Theiler’s virus myelitis
synthesized and the cells responding. Th0 cells may be
precursors of Th1 and Th2 cells.
T h1 cells
A murine and human CD4 + T cell subset based on cytokine
production and effector functions. Th1 cells synthesize
interferon-γ (IFN-γ), IL2, and tumor necrosis factor β
(TNF-β). They are mainly responsible for cellular
immunity against intracellular microorganisms and for
delayed-type hypersensitivity reactions. They affect IgG 2a
antibody synthesis and antibody-dependent, cell-mediated
cytotoxicity. Th1 cells activate host defense mediated
by phagocytes. Intracellular microbial infections induce
Th1 cell development, which facilitates elimination of the
microorganisms by phagocytosis. Th1 cells induce synthesis
of antibody, which activates complement and serves as an
opsonin that facilitates phagocytosis. The IFN-γ they produce
enhances macrophage activation. The cytokines released by
Th1 cells activate natural killer (NK) cells, macrophages, and
CD8 + T cells. Their main function is to induce phagocytemediated
defense against infections, particularly by intracellular
microorganisms. Also termed inflammatory T cells.
T h2 cells
A murine and human CD4 + T cell subset based on cytokine
production and effector functions. Th2 cells synthesize
interleukin-4 (IL4), IL5, IL6, IL9, IL10, and IL13. Their
main function is to induce antibody synthesis by B cells.
They greatly facilitate IgE and IgG 1 antibody responses and
mucosal immunity by synthesis of mast cell and eosinophil
growth and differentiation factors and facilitation of
IgA synthesis. IL4 facilitates IgE antibody synthesis. IL5
is an eosinophil-activating substance. IL10, IL13, and IL4
suppress cell-mediated immunity. Th2 cells are principally
responsible for host defense exclusive of phagocytes. They
are crucial for IgE and eosinophil responses to helminths
and for allergy attributable to activation of basophils and
mast cells through IgE.
T h17 (hypothesis)
A concept to explain T cell-mediated tissue injury including
organ-specific autoimmunity triggered by microbial
infection. The identification of novel cytokines of the IL17
and IL12 families has permitted identification of factors
that specify differentiation of a new effector T cell lineage
known as T h17 that provides a new mechanism of adaptive
immunity and a unifying model to explain many aspects
of immune regulation, immune pathogenesis, and host
defense. The T h17 pathway involves the actions of pleiotropic
cytokines including transforming growth factor-β
(TGF-β) and IL6. IL17 is a T cell-expressed pleiotropic
cytokine that exhibits a high degree of homology to a protein
encoded by the ORF13 gene of herpes virus Saimiri.
Both recombinant and natural IL17 occur as disulfide
linked homodimers. IL17 exhibits multiple biological
activities on a variety of cells, including the induction of
IL6 and IL8 production in fibroblasts, activation of NF-κB,
and costimulation of T cell proliferation. IL17 is an essential
inflammatory mediator in the development of autoimmune
diseases. Neutralization of IL17 with monoclonal antibody
can ameliorate the disease course. Also called CTLA-8.
thalidomide
An immunomodulatory agent whose effects vary under
different conditions, but may be related to suppression of
excessive TNF-α synthesis and downmodulation of selected
cell surface adhesion molecules involved in leukocyte
migration. A drug originally used as a sedative, it was
withdrawn in the 1960s as a consequence of disastrous
teratogenic effects when used during pregnancy. However,
it is again in use because of its significant immunomodulatory
effects. It inhibits angiogenesis and exerts antiinflammatory
and immunomodulatory actions. It inhibits
tumor necrosis factor α (TNF-α), diminishes phagocytosis
by neutrophils, increases IL10 synthesis, alters expression
of adhesion molecules, and facilitates cell-mediated
immunity through interaction with T cells. Presently used
to treat multiple myeloma, it has potential for treatment of
myelodysplastic syndrome, acute myelogenous leukemia
and graft-vs.-host disease. Toxicities include teratogenesis,
peripheral neuropathy, constipation, fatigue, rash, hypothyroidism,
and increased risk of deep vein thrombosis.
Max Theiler.
Theiler, Max (1899–1972)
South African virologist who received a Nobel Prize
in 1951 for his development of vaccines against yellow
fever.
Theileria immunity
Immunity against these tick-transmitted intracellular
protozoan parasites of domestic animals depends upon the
protection of cell-mediated immune responses. Humoral
immune responses directed against schizonts and piroplasms
are insignificant in the development of natural protective
immunity. Animals that recover may be resistant to
homologous challenge and develop immunity that persists
3 to 5 years. Infection with sporozoites and the development
of schizonts are critical for the development of natural
immunity. Live attenuated, subunit, and recombinant
vaccines have been used. Theileria annulata live vaccine
is prepared from attenuated cell lines that produce infection
in cattle without causing disease and induce protective
immunity. T. parva subunit vaccine contains p67 antigen,
the recombinant form of which protects 70% of immunized
cattle against experimental challenge.
Theiler’s virus myelitis
Murine spinal cord demyelination considered an immunebased
consequence of a viral infection.
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