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Sm, Berney; Schaan, T; Re, Wolf; Dl, Kimpel; H, van der Heyde; Tp, Atkinson

doi:10.1023/a:1010919719200

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…As CD5 physically associates with TCRζ/CD3 complex upon TCR and pMHC interaction, the tyrosine residues in both TCRζ and CD5 are phosphorylated by tyrosine kinases associated with the complex [ 30 , 106 , 107 , 108 , 109 , 110 ]. This interaction is so intrinsic to T cell signaling that CD5 expression levels are proportional to the degree of TCRζ phosphorylation, IL-2 production capacity, and ERK phosphorylation which are critical for CD3-mediated signaling [ 33 , 111 ]. It is unknown whether posttranslational modifications, such as conserved domain 1 and domain 2 glycosylations, impact CD5 signaling [ 112 , 113 ].…”

Section: Cd5: a Contradictory Co-receptormentioning

confidence: 99%

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T Cell Calcium Signaling Regulation by the Co-Receptor CD5

Freitas

Johnson

Weber

2018

IJMS

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Calcium influx is critical for T cell effector function and fate. T cells are activated when T cell receptors (TCRs) engage peptides presented by antigen-presenting cells (APC), causing an increase of intracellular calcium (Ca2+) concentration. Co-receptors stabilize interactions between the TCR and its ligand, the peptide-major histocompatibility complex (pMHC), and enhance Ca2+ signaling and T cell activation. Conversely, some co-receptors can dampen Ca2+ signaling and inhibit T cell activation. Immune checkpoint therapies block inhibitory co-receptors, such as cytotoxic T-lymphocyte associated antigen 4 (CTLA-4) and programmed death 1 (PD-1), to increase T cell Ca2+ signaling and promote T cell survival. Similar to CTLA-4 and PD-1, the co-receptor CD5 has been known to act as a negative regulator of T cell activation and to alter Ca2+ signaling and T cell function. Though much is known about the role of CD5 in B cells, recent research has expanded our understanding of CD5 function in T cells. Here we review these recent findings and discuss how our improved understanding of CD5 Ca2+ signaling regulation could be useful for basic and clinical research.

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Section: Cd5: a Contradictory Co-receptormentioning

confidence: 99%

“…Thus, CD5 has a mix of downstream effects that both promote and inhibit T cell activation. Curiously, recent work suggests that in contrast to its initial inhibitory nature, CD5 also co-stimulates resting and mature T cells by augmenting CD3-mediated signaling [ 25 , 33 , 34 , 35 ].…”

Section: Introductionmentioning

confidence: 99%

T Cell Calcium Signaling Regulation by the Co-Receptor CD5

Freitas

Johnson

Weber

2018

IJMS

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“…However, differences exist between CD4 + and CD8 + T cell subsets and impact of cell isolation protocols, sample storage, and mitogen selection have been shown. 16,17 The aim of this study was to evaluate applicability of chicken homologs to well-known mammalian markers: CD25; 17,18 CD28 19 CD5; 20,21 MHC-II; 22 CD44; 23,24 and CD45, 25,26 in the assessment of chicken T cell activation in response to concanavalin A (Con A) stimulation.…”

mentioning

confidence: 99%

Kinetics of activation marker expression after in vitro polyclonal stimulation of chicken peripheralT cells

et al. 2021

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A comprehensive analysis of T cell activation markers in chicken is lacking. Kinetics of T cell activation markers (CD25, CD28, CD5, MHC-II, CD44, and CD45) in response to in vitro stimulation of peripheral blood mononuclear cells with concanavalin A (Con A) were evaluated between two chicken lines selected for high and low levels of mannose-binding lectin in serum (L10H and L10L, respectively) by flow cytometry. L10H chickens showed a stronger response to Con A based on the frequency of T cell blasts in both the CD4 + and CD8 + compartment. The majority of the proliferating CD4 + and CD8 + T cells expressed CD25. Proliferating T cells were seen both in the CD4 + MHC-II +/− and CD8 + MHC-II +/− population. For both CD4 + and CD8 + T cells, frequencies of CD25 + and MHC-II + T cells were increased 24 h after stimulation. CD28 + frequencies were only increased on CD8 + T cells 48 h after stimulation. An increase in the relative surface expression based on mean fluorescence intensity (MFI) upon activation was observed for most markers except CD5. For CD4 + T cells, CD28 expression increased 24 h after stimulation whereas MHC-II expression increased after 48 h. For CD8 + T cells, a tendency toward an increase in CD25 expression was observed. CD28 expression started to increase 24 h after stimulation and only a transient peak in MHC-II expression on CD8 + T cells was observed after 24 h. CD44 and CD45 expressed on CD4 + and CD8 + T cells increased 24-72 h after stimulation. In summary, the frequency of CD25 + and MHC-II + T cells were shown to be early markers (24 h) for in vitro activation of both CD4 + and CD8 + T cells. Frequency of CD28 + T cells was a later marker (48 h) and only for CD8 + T cells.Surface expression of all markers (MFI) increased permanently or transiently upon activation except for CD5.

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Alefacept selectively promotes NK cell‐mediated deletion of CD45R0⁺ human T cells

et al. 2003

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Modulation of the immune response using immunoglobulin fusion proteins has shown great promise for clinical immunotherapy of autoimmune diseases. Alefacept is an immunoglobulin fusion protein composed of the first extracellular domain of human LFA-3 fused to the hinge, C H 2 and C H 3 domains of human IgG 1 . Alefacept has previously been reported to inhibit T cell proliferation. Here, we analyzed the effects of alefacept on lymphocytes in vitro and characterized the role of autologous NK cells in its mechanism of action. Alefacept, but not a C H 2 binding mutant of Alefacept, inhibited CD3-induced T cell proliferation only in the presence of live NK cells, consistent with an important role for Fc + R engagement. Alefacept caused preferential depletion of CD69+ T cell subsets. Cytotoxicity assays revealed that alefacept, but not the C H 2 binding mutant, induced NK cell-mediated death of activated T cells and sorting into CD45R0 + and CD45RA + subpopulations showed that lymphocyte deletion occurred preferentially in the CD45R0 + subset. Activated CD45R0 + cells expressed higher levels of CD2 than CD45R0 -cells, providing a possible explanation for the selective targeting of this subset. Our results suggest that selective targeting of CD45R0 + T cells by NK cells represents a potential therapeutic mechanism of action of alefacept.

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Untitled

Cited by 5 publications

References 27 publications

T Cell Calcium Signaling Regulation by the Co-Receptor CD5

T Cell Calcium Signaling Regulation by the Co-Receptor CD5

Kinetics of activation marker expression after in vitro polyclonal stimulation of chicken peripheralT cells

Alefacept selectively promotes NK cell‐mediated deletion of CD45R0⁺ human T cells

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Untitled

Cited by 5 publications

References 27 publications

T Cell Calcium Signaling Regulation by the Co-Receptor CD5

T Cell Calcium Signaling Regulation by the Co-Receptor CD5

Kinetics of activation marker expression after in vitro polyclonal stimulation of chicken peripheralT cells

Alefacept selectively promotes NK cell‐mediated deletion of CD45R0+ human T cells

Contact Info

Product

Resources

About

Alefacept selectively promotes NK cell‐mediated deletion of CD45R0⁺ human T cells