Functional expression of human CD28 in murine T cell hybridomas

Couez, Dominique; Pagès, Françoise; Ragueneau, Marguerite; Nunès, Jacques A.; Klasen, Sandrine; Mawas, Claude; Truneh, Alemseged; Olive, Daniel

doi:10.1016/0161-5890(94)90137-6

Cited by 15 publications

(7 citation statements)

References 43 publications

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“…Interestingly, we also found that CD28 costimulation induces a drastic increase of CD3-induced PLCg1 phosphorylation and Ca 2þ flux. The CD28 CsA-sensitive pathway is mainly limited to T cells of the CD4 þ subset 33 and dominant in activated T cells 34,35 in which the [Ca 2þ ] i increase is preferentially induced by CD80-mediated stimulation of CD28. Even if molecular mechanisms underlying costimulation are largely unknown, new findings show that CD28 does not lead to increased Zap-70/LAT phosphorylation but amplifies PLCg1 phosphorylation (and thus Ca 2þ flux) through Itk activation.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic T lymphocyte‐associated antigen‐4 inhibits integrin‐mediated stimulation

et al. 2002

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SUMMARYThe negative role exerted by cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) in the regulation of T-cell activity, as induced by T-cell receptor (TCR)/CD3 and CD28 costimulation, has been widely described. In the present work we investigated the role of CTLA-4 in the control of cell activation, as induced by costimulation of the adhesion molecule lymphocyte functionassociated antigen-1 (LFA-1) in murine CD4þ T cells. Results show that CTLA-4 engagement inhibits interleukin-2 (IL-2) production, not only when induced by CD3/CD28 costimulation, but also when CD4 þ T cells are costimulated by anti-CD3 and anti-LFA-1 monoclonal antibodies (mAbs). LFA-1 has been described to induce Ca 2þ mobilization also in the absence of TCR engagement. Moreover, we found that CTLA-4 engagement negatively affects Ca 2þ mobilization and NF-AT activation, as induced by LFA-1 engagement alone. PLCg1 phosphorylation was also dampened within minutes after CTLA-4 engagement. Altogether these data indicate that through the control of signals induced by different receptors, CTLA-4 could be a global attenuator of T-cell activation.

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Section: Discussionmentioning

confidence: 99%

Cytotoxic T lymphocyte‐associated antigen‐4 inhibits integrin‐mediated stimulation

et al. 2002

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“…Although occupancy and oligomerization of CD28 alone leads to a response detectable at the biochemical level , and some CD28-specific mAb induce IL-2 secretion in tumor cell lines [22,23], induction of T cell proliferation in resting Tcells is thought to strictly depend on TCR engagement. As a basis for the cooperation between TCR and CD28-mediated signals, evidence for the convergence of TCR and CD28-induced signaling cascades in the activation of transcription factors required for IL-2 synthesis has been provided [24].…”

Section: Introductionmentioning

confidence: 99%

CD28‐mediated induction of proliferation in resting T cells in vitro and in vivo without engagement of the T cell receptor: Evidence for functionally distinct forms of CD28

et al. 1997

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JJ316 and JJ319 are rat CD28-specific monoclonal antibodies (mAb) of the gamma1 kappa isotype with identical co-stimulatory potency. At a concentration 100-1000-fold higher than that required for co-stimulation, JJ316, but not JJ319 induces massive proliferation of all T cell subsets in vitro without T cell receptor (TCR) triggering. "Direct" stimulation by JJ316 is fully blocked by JJ319, indicating that it is not due to cross-reactivity of JJ316 with the TCR complex or other activating receptors. JJ316 binds much more slowly to primary T cells than JJ319, whereas both antibodies bind with similar kinetics to CD28-transfected L-929 cells, suggesting that JJ316 binding to T cells requires redistribution or a conformational change of CD28. In vivo, JJ316 but not JJ319 induces rapid and transient proliferation of most CD4 T cells and, indirectly, of B cells. These data show that TCR engagement is not an absolute prerequisite either in vitro or in vivo for the induction of T cell proliferation through CD28 and suggest that mAb JJ316 is able to stimulate resting T cells directly by recruiting CD28 molecules from an inactive to an active form.

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“…D3Res glioma cells as previously described (Couez et al, 1994). Twenty-four hr after transfection, 5 x 10 4 cells were seeded in each well of a 24-well tissue culture plate, and grown in F12-10% FCS supplemented with 3 mg/ml Abbreviations CNS…”

Section: Plasmid Construction and Transfectionsmentioning

confidence: 99%

“…A 2.1-kb fragment of the rat VDR cDNA (Burmester et al, 1988) was introduced into the mammalian expression vector, pH␤act-Neo, and was transfected by protoplast fusion (Couez et al, 1994) into the C6.4 D3Res cell clone. As a control, cells of sister cultures were transfected with the vector alone.…”

Section: Stable Transfection Of Vdr Cdna Into C64 D3res Cellsmentioning

confidence: 99%

Vitamin D receptor stable transfection restores the susceptibility to 1,25-dihydroxyvitamin D3cytotoxicity in a rat glioma resistant clone

et al. 1998

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Recently, 1,25-dihydroxyvitamin D3 (1,25-D3) and less hypercalcemic analogs were shown to exert a delayed cytotoxic effect on rat C6 glioma cells. 1,25-D3 induces in these cells a programmed cell death, accompanied by the induction of c-myc, p53 and gadd 45 genes. The involvement of the intracellular vitamin D receptor (VDR) remained to be determined. In this lethal process, we have investigated its role in a subclone of C6 cells, which was isolated on the basis of its resistance to 1,25-D3, and in which VDR expression was not detected either at the mRNA or protein levels. The stable transfection of a rat VDR cDNA into this clone restored its susceptibility to the cytotoxic effects of 1,25-D3. This phenomenon was accompanied by a dramatic upregulation of c-myc mRNA expression, as already described in a C6-sensitive clone. These results provide the first evidence that VDR expression, if not sufficient, is necessary to mediate 1,25-D3 cytotoxic effect in C6 glioma cells. Since VDR mRNA expression has been already reported in human brain tumors, our data imply that the identification of VDR expression could become a prerequisite in any strategy of glioma treatment with vitamin D analogs.

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Functional expression of human CD28 in murine T cell hybridomas

Cited by 15 publications

References 43 publications

Cytotoxic T lymphocyte‐associated antigen‐4 inhibits integrin‐mediated stimulation

Cytotoxic T lymphocyte‐associated antigen‐4 inhibits integrin‐mediated stimulation

CD28‐mediated induction of proliferation in resting T cells in vitro and in vivo without engagement of the T cell receptor: Evidence for functionally distinct forms of CD28

Vitamin D receptor stable transfection restores the susceptibility to 1,25-dihydroxyvitamin D3cytotoxicity in a rat glioma resistant clone

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