Biomedical Engineering Reference
In-Depth Information
T H22 Cell
CD4
, IL22-producing helper T cells (T H22 ) constitute an additional T H cell subset.
Production of interleukin-22 depends less on the transcription factor retinoic acid
receptor-related orphan receptor-gamma2 (or NR1f3-2) than that of IL17 cytokine.
Synthesis of IL22 relies on transcription factor aryl hydrocarbon receptor (AHR or
class-E basic helix-loop-helix protein bHLHe76).
T H22 cells can be generated in vitro from naive CD4
+
T cells subjected to
IL6 and tumor-necrosis factor [ 258 ]. Plasmacytoid dendritic cells support more
efficiently T H22 cell differentiation than conventional dendritic cells. Binding
partners of bHLHe76 factor favor the differentiation into T H22 cells from naive
T cells [ 259 ].
This subset of human T cells is characterized by the expression of skin-homing
chemokine receptors, such as CCR4 and CCR10. Expression of CCR10 depends
on the presence of active vitamin-D3 metabolites. However, T H22 cells do not
synthesize interleukin-17 and interferon-
+
[ 258 ]. 126
γ
3.10.4.7
Cytotoxic T Lymphocytes
Cytolytic T lymphocytes (CTL) express T-cell receptor and its coreceptor cluster
of differentiation CD8 for recognition of a complex formed by antigen and class-
1 major histocompatibility complex molecule. After antigenic stimulation, CD8
+
CTLs enter into a transient state characterized by reduced antigen-HLA binding
despite normal plasmalemmal amounts of TCR and CD8. This decrease in activity
several days after antigenic stimulation results from the loss of colocalization of
T-cell receptor and CD8.
Galectin-glycan lattices on the cell surface formed from galectin-3 and
-
galactoside regulate the formation of focal adhesions 127 and disrupt the association
of T-cell receptor with CD8 in cytolytic T lymphocytes [ 260 ]. 128
β
T-cell receptor
becomes colocalized with galectin-3.
126 Interleukin-22 is produced mainly by T H17 cells and some natural killer cell-like subsets (NK22)
subset of natural killer cells that acts on epithelial cells and keratinocytes of mucosal surfaces.
127 Migrating cells communicate with the extracellular matrix via focal adhesions that are formed
by integrins, phosphorylated caveolin-1, Glc N Ac transferase-5 (GAT5), and focal adhesion kinase.
Caveolin-1 serves as plasmalemmal adaptor that promotes integrin signaling via Src and FAK
kinases. Galectin plasmalemmal nanodomain recruits glycoproteins depending on N glycan number
and branching, a feature determined by Glc N Ac transferase-5. Galectin-3 bound to GAT5-processed
N glycans and phosphorylated caveolin-1 cooperate to stabilize focal adhesion kinase [ 261 ].
128 Galectin-glycan lattices restrict the lateral mobility of cell-surface glycoproteins, thereby
inducing stable membrane structures. The formation of galectin-glycan lattices is regulated by
N acetylglucosaminyltransferases that synthesize
β
-galactosides, which serve as terminal carbohy-
drates of N glycans.
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