Exact(27)
Accumulating evidence suggests that brain infiltrating T cells during ECM are strongly activated and differentiated memory cells [1].
A previous study of ECM has demonstrated that brain infiltrating T cells are strongly activated and are CD44+CD62L− differentiated memory T cells [1].
Our findings indicate that memory CD8+ T cells in persons with neuroinvasive disease were memory T cells are skewed towards a terminally differentiated, memory phenotype that was predominately monofunctional.
We were particularly interested in measuring the proportion of T cells expressing OX40 because a large portion of brain infiltrating CD4+ and CD8+ T cells have been shown to be differentiated memory T lymphocytes during ECM [1].
For the purposes of this study, the phenotypes of TEMRA+ and TEM cells as described above would predominantly define fully differentiated memory cells that are CD27− but IL-7Rα+.
Tregs from human skin are highly proliferative in vivo, develop alongside effector responses at the site of a skin inflammation [321], and can be induced in vivo and ex vivo from highly differentiated memory T cells, by antigen reencounter [321], [322].
Similar(33)
Within the T-cell compartment, end-differentiated memory and effector T cells replace naïve T cells.
Thus, the reason for much of this shift in T cell subpopulations towards CD8+ T cells terminally-differentiated memory cells may be infectious (Pawelec et al 2004).
Conversely, effector memory (TEM) and terminally-differentiated memory cells (TTD) have lost CCR7 expression, can traffic to peripheral sites, and are characterized by immediate effector capacities such as cytokine secretion and cytotoxic activity [ 13].
End-differentiated memory T cells in RA frequently acquire expression of the fractalkine receptor CX3CR1 (chemokine [C-X3-C motif] receptor 1) [ 87], as well as regulatory receptors that are usually found on natural killer cells, such as natural-killer group 2, member D (NKG2D) and killer immunoglobulin-like receptors [ 88- 90].
These findings are somewhat surprising on the basis of our previous study of CD8 T-cell phenotype in children with TB, where the antigen-specific CD8 T-cell distribution pattern consistently changed four months after therapy, with a significant recovery of terminally differentiated effector memory T-cells and decreased frequencies of central memory T-cells [14].
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