Biomedical Engineering Reference
In-Depth Information
Table 3.24.
Markers and transcription factors of T-lymphocyte populations (
Part 3
;
Source: [
225
]; BLIMP: B-lymphocyte-induced maturation protein; BTLA: B- and T-lymphocyte
attenuator; CBL: Casitas B-lineage lymphoma; CD3(8): cluster of differentiation-3(8), or T-
cell coreceptor; CKI: cyclin-dependent kinase inhibitor; CTLA: cytotoxic T-lymphocyte an-
tigen [CTLA4 is also called CD152]; EOMES: eomesodermin; Fox: forkhead box; GITR:
glucocorticoid-induced TNF-receptor related protein, or TNFRSF18; GRAIL: gene related to
anergy in lymphocytes; J: joining region; LAG: lymphocyte activation gene; MAIT: mucosal-
associated invariant T cell; MR: MHC-related protein; NEDD: neuronal precursor cell-expressed
developmentally downregulated; NKT: natural killer T cell; PD: programmed cell death; PLZF:
promyelocytic leukemia zinc finger protein, a.k.a. zinc finger and BTB domain-containing protein
ZBTB16 and zinc finger protein ZNF145; SAP: SLAM-associated protein; SLAM: signaling
lymphocytic activation molecule; SLAMF: signaling lymphocytic activation molecule family
member; SMAD: small mothers against decapentaplegic homolog; STAT: signal transducer and
activator of transcription; TBx: T-box transcription factor; TCR: T-cell receptor; TIM: T-cell
immunoglobulin and mucin domain protein; V: variable region).
Subset
Plasmalemmal markers and transcription factors
Cytotoxic
αβ
TCR, CD3, CD8; EOMES, TBx21, BLIMP1
mainly CD45Ro (PTPRc, CD45
lMW
),
some CD45Ra (PTPRc; CD45
hMW
)
T
R1
αβ
TCR, CD3, IL16R
Natural T
Reg
αβ
TCR, CD3, IL16R, CD25, CTLA4, TNFRSF18;
(nT
Reg
)
FoxO1/O3/P3, STAT5
Inducible T
Reg
αβ
TCR, CD3, IL16R, CD25, CTLA4, TNFRSF18;
(iT
Reg
)
FoxO1/O3/P3, SMAD2-SMAD4, STAT5
NKT
CD1-restricted TCR; KLRb1c, SLAMF1/6, T
β
R;
PLZF
α
α
MAIT
MR1-restricted; V
7.2, J
19
Anergic
αβ
TCR, CD3, BTLA; CKI1b
Exhausted
CD3, CD8, PD1, TIM3, LAG3; SAP; BLIMP1
the differentiation program in selected thymocytes lead to the specific lineages
of mature T cells. The development of
αβ
T cells requires rearrangement of
the loci that encode T-cell antigen receptor-
α
and -
β
and appropriate signals
via interactions between TCRs on double-positive CD4
thymocytes and
peptide in the context of major histocompatibility complex (MHC) molecules on
thymic stromal cells. Double-positive CD4
+
,CD8
+
thymocytes that successfully
rearrange genes encoding T-cell antigen receptors in fact mature into single-positive
CD4
+
,CD8
+
cytotoxic T cells whether TCRs are specific for MHC
molecules of class-2 or -1, respectively. In addition, TCR signal duration during
selection determines lineage type, as signals of short and long duration cause
CD8
+
helper or CD8
+
differentiation, respectively. Prolonged engagement of MHC
class-2-restricted TCRs followed by sustained cellular signaling is needed for the
development of the helper lineage. MHC class-1 and -2 molecules lead to signals of
short and long duration, as TCR signals in double-positive thymocytes block MHC
class-1-dependent signaling, but not MHC class-2-dependent signaling.
+
and CD4
+
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