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T cell domains 684 T cell priming
cortex to the medulla. As maturation proceeds, CD4 – /
CD8 – (double-negative) T cells develop into CD4 + /CD8 +
and become CD4 – /CD8 – or CD4 – /CD8 + single-positive
T cells. Somatic rearrangement of variable, diversity (β),
and joining gene segments in the area of C gene segments
leads to the production of functional genes that encode
TCR γ and δ polypeptides. Many T cell specificities result
from the numerous combinations possible for joining
separate gene segments in addition to various mechanisms
for junctional diversity. Somatic rearrangement
of germline genes is also responsible for the functional
genes that encode TCR α and β polypeptides. While fewer
V genes are in the γ and δ loci and junction diversity is
greater, the mechanisms to produce γδ diversity resemble
those for the αβ receptor. A few cortical thymocytes
express γδ receptors. Thereafter, a line of developing T
lymphocytes expresses numerous αβ TCR receptors. The
β chains appear first, followed by α chains of TCRs. The
β chain associates with an invariant pre-T α surrogate α
chain. Signals transduced by the pTαβ receptor facilitate
expression of CD4 and CD8 and facilitate expansion of
immature thymocytes. CD4 + /CD8 + cortical thymocytes
first express αβ receptors. Self major histocompatibility
complex (MHC) restriction and self tolerance develop as
consequences of the interactions of cortical epithelial cells
and nonlymphoid cells derived from the bone marrow that
both express MHC. This leads to selection of T cells to
be saved. During positive selection, CD4 + /CD8 + TCR αβ
thymocytes recognize peptide–MHC complexes on thymic
epithelial cells with low avidity. This saves them from
programmed cell death (apoptosis). Recognition of self
peptide–MHC complexes on thymic antigen-presenting
cells with avidity by CD4 + /CD8 + TCR αβ thymocytes
leads to apoptosis. Most cortical thymocytes are killed
during selection. The αβ thymocytes that remain undergo
maturation and proceed to the medulla, where they
become CD4 + /CD8 – or CD4 – /CD8 + single-positive cells.
During residence in the medulla, they become helper or
cytolytic cells prior to their journey to the peripheral lymphoid
tissues, where they function as self MHC-restricted
helper T cells or precytotoxic T lymphocytes capable of
responding to foreign antigen.
T cell domains
Specific areas in lymph nodes and other lymphoid organs
where T lymphocytes localize preferentially.
T cell growth factor (TCGF)
Refer to interleukin-2 (IL2).
T cell growth factor 1
Interleukin-2 (IL2).
T cell growth factor 2
Interleukin-4 (IL4).
T cell help
Facilitation through cytokines and costimulatory signals or
B cell and cytotoxic T cell activation by T helper cells. Th1
and Th2 cytokines facilitate antibody isotype switching in
B cells.
T cell hybridomas
The immortalization of normal T lymphocytes by fusion
with continuously replicating tumor cells. Fusion randomly
immortalizes T lymphocytes regardless of their
antigen specificity and genetic restrictions to form a T cell
hybridoma. This represents one of two methods to isolate
and propagate T cell lines in clones of defined specificity.
The other technique is to span clones of normal immune
T lymphocytes stimulated with appropriate antigens and
antigen-presenting cells. The hybridoma technique has an
advantage over T cell cloning in the relative ease in securing
relatively large numbers of T cells of interest and their
biologically active products. Lymphokines and other regulatory
molecules along with their nRNA and DNA represent
T cell hybridoma products. This technology has facilitated
evaluation of T cell receptors and their antigen recognition
mechanisms. The adoptive (passive) transfer of autoantigenspecific
T cell hybridomas in mice can induce autoimmune
diseases.
T cell immunodeficiency syndrome (TCIS)
Decreased immune function as a consequence of complete
or partial defects in T lymphocyte functioning.
Patients develop recurrent opportunistic infections and
may manifest cutaneous anergy, wasting, diminished life
expectancy, growth retardation, and increased likelihood
of developing graft-vs.-host disease. They may
have serious or even fatal reactions following immunization
with BCG or live virus vaccines and face increased
likelihood of malignancy. T cell immunodeficiencies are
usually more profound than B cell immunodeficiencies
and have no effective treatment. This group of disorders
includes thymic hypoplasia (DiGeorge syndrome), cellular
immunodeficiency with immunoglobulins, and defects of
T lymphocytes caused by deficiency of purine nucleoside
phosphorylase and lack of inosine phosphorylase.
T cell-independent (TI) antigen
An immunogen that is simple in structure, often a polysaccharide
such as the polysaccharide of the pneumococcus,
a dextran polyvinyl hooter, or a bacterial lipopolysaccharide.
This antigen elicits an IgM response only and fails to
stimulate an anamnestic response. It is not found in most
pathogenic microbes.
T cell leukemia
Adult T cell leukemia/lymphoma.
T cell leukemia viruses
Retroviruses such as HTLV-I (human T lymphocyte virus
I) that induce human T cell leukemia, and HTLV-II, which
has been associated with hairy cell leukemia.
T cell lymphoma (TCL)
Neoplastic proliferation of T lymphocytes diagnosed by
determining whether rearrangement of the genes encoding
the T lymphocyte receptor β chain has occurred.
T cell maturation
Refer to thymus cell differentiation figure.
T cell migration
Cells leaving the thymus migrate to all peripheral lymphoid
organs seeding in the T-dependent regions of the lymph
nodes and spleen and at the peripheries of lymphoid follicles.
The rate of release of thymocytes from the thymus
increases markedly after antigenic stimulation. The patterns
of migration of T cells and B cells have been studied by
adoptive transfer of labeled purified cells into irradiated
syngeneic mice matched for age and sex.
T cell non-antigen-specific helper factor
A substance that provides nonspecific help to T lymphocytes.
T cell priming
Mature naïve T cell stimulation by antigen presented to
them by professional antigen-presenting cells.