Anti‐CD2 (sheep red blood cell receptor) monoclonal antibodies and T cell activation I. Pairs of anti‐T11.1 and T11.2 (CD2 subgroups) are strongly mitogenic for T cells in presence of 12‐O‐tetradecanoylphorbol 13‐acetate

Olive, Daniel; Ragueneau, Marguerite; Cerdan, Chantal; Dubreuil, Patrice; Lopez, Marc; Mawas, Claude

doi:10.1002/eji.1830160906

Cited by 76 publications

(26 citation statements)

References 20 publications

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“…Induction of T-cell activation via T11 surface molecule requires appropriate combinations of mAbs directed against different epitopes of the molecule (5). We used two different combinations of anti-T11 mAbs that had previously been shown to induce optimal production of IL-2 from JA3 in the presence of PMA (13,16). As shown in Table 3, all T3-Ti-T44+ Leu-1+ T11+ variants were responsive to anti-T11-mediated stimulation.…”

Section: Resultsmentioning

confidence: 99%

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Selection and characterization of T-cell variants lacking molecules involved in T-cell activation (T3 T-cell receptor, T44, and T11): analysis of the functional relationship among different pathways of activation.

Moretta¹,

Poggi

Olive³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

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A clone of the interleukin 2-producing Jurkat leukemia cell line termed JA3 (surface phenotype, T31, Ti+, T44+, T11+, T40+) has been used to induce and select cell variants lacking surface molecules involved in T-cell activation.Following 200 rad of V-radiation (1 rad = 0.01 Gy), cells were treated with monoclonal antibodies (mAbs) directed to T3, Ti, T44, or T11 antigen and complement. (3,4), it has been shown that the combined use ofmAbs directed to distinct epitopes ofthe T11 molecule leads to T-cell activation (5). The third pathway of T-cell activation is initiated by the T44 cell-surface glycoprotein after interaction with specific mAbs (6, 7). Recent studies have been aimed at understanding the functional relationship existing among the three distinct pathways of T-cell activation. A major finding was that mAb-induced modulation of the T3-Ti antigen receptor complex led to unresponsiveness not only to anti-T3 or anti-Ti mAbs but also to anti-T11 (5) or anti-T44 mAbs (6). These results suggested that both T11 and T44 pathways of activation may be "regulated" by surface expression of the T-cell receptor complex.A useful approach to better define the functional and physical relationship among different surface molecules involved in human T-cell activation is represented by the study of "functional" T-cell lines and their variants. This approach has been recently applied by Weiss and Stobo (8) to the analysis of T3-Ti negative variants derived from the interleukin 2 (IL-2)-producing Jurkat leukemic T-cell line.In the present study, we analyzed the functional capability of phenotypically distinct cell variants derived by immunoselection with mAb and complement from the IL-2-producing JA3 cell line (9) following low dosages of irradiation. JA3 cells do not express detectable T4 or T8 surface antigens and exhibit the T3' Ti+ T44' Leu-1+ T11' T40' (3A1) 4F2' HLA class I' surface phenotype.Variants obtained by immunoselection with mAbs directed against T3 or Ti surface molecules were characterized by the simultaneous loss of both surface molecules. The second group was obtained by negative selection against the T44 surface antigen: the resulting T44-variants were also found to lack T3, Ti, and Leu-1 antigens. The third set of variants was obtained by immunoselection against surface T11 antigen: all the variants lacked all T-cell-specific markers but they still expressed 4F2 and HLA class I antigens. These data suggest the existence of a coordinated expression of surface T-cell antigens similar to that occurring at discrete stages of intrathymic differentiation (10). Functional studies of the three distinct sets of variants indicated that the T44 pathway of activation is functionally dependent on the "classical" pathway initiated by the T3-Ti receptor complex. In contrast and in partial disagreement with previous conclusions based Abbreviations: mAb, monoclonal antibodies; IL-2, interleukin 2; PMA, phorbol 12-myristate 13-acetate; PHA, phytohemagglutinin.The publication costs of this article were defrayed ...

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Section: Resultsmentioning

confidence: 99%

“…Anti-Leu-1 mAb was purchased from Becton Dickinson. Stimulatory anti-T11 mAbs (CD2-1, CD2-9, MAR 206) were derived as described (12,13), whereas the 9.6 mAb (also recognizing the T11 antigen) was purchased from New England Nuclear. The JTi2 mAb recognizing the T-cell receptor of JA3 cells has been described in detail elsewhere (9,14).…”

mentioning

confidence: 99%

Selection and characterization of T-cell variants lacking molecules involved in T-cell activation (T3 T-cell receptor, T44, and T11): analysis of the functional relationship among different pathways of activation.

Moretta¹,

Poggi

Olive³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

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“…32 For this reason, 2 different antibodies to CD2 were chosen, clones 4B2, CLB-T11/1 and 4B2, CLB-T11.2/1. However, the frequency of MTOC polarization in CD4 ϩ control T Anti-CD25 (IL-2R␣) 3 1.31 (25) 18.3 (6) .006…”

Section: Cross-linking Of Certain T-cell Surface Molecules Leads To Pmentioning

confidence: 99%

Engagement of specific T-cell surface molecules regulates cytoskeletal polarization in HTLV-1–infected lymphocytes

Barnard

Igakura

Tanaka

et al. 2005

Blood

106

112

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“…19,20 In agreement with the latter investigators, we found that a pair of mAb directed to two different epitopes of the CD2 molecule (T11.1 + T11.2) was highly active in triggering T cells in the absence of antigen-presenting cells or phorbol ester. 21 Combining this pair of CD2 mAb resulted in stimulation of both naive and memory T cells, respectively. Addition of TGF-b 1 , known to exert a costimulatory effect on CD4 + CD45RA + naive T cells, 22 enhanced CD2-mediated development of CD7 7 memory cells whereas other cytokines showed no effect.…”

mentioning

confidence: 99%

CD7‐negative T cells represent a separate differentiation pathway in a subset of post‐thymic helper T cells

et al. 1996

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SUMMARYThe absence of CD7 protein and the corresponding mRNA is a stable feature in a subset of normal circulating CD4 memory T cells. It is still unresolved whether the CD7 ÿ subset represents a specific Tcell lineage. Here we show that repeated stimulation of highly purified CD4 CD45RA CD45RO ÿ naive T cells in vitro leads to the development of a distinct memory subset that is defined by the expression versus non-expression of the CD7 antigen. Comparing different T-cell activation pathways (TCR/CD3, CD2), we observed that alternative signals were critically involved in the development of CD4 + CD7 ÿ T cells. Peak mean numbers of CD7 ÿ memory cells occurred after 3-5 cycles of restimulation in vitro. Naive T cells that had undergone repeated stimulations were harvested and sorted into CD7and CD7 ÿ subsets. The vast majority (> 97%) of CD7 T cells retained their expression, whereas the CD7 ÿ population did not re-express the antigen during further propagation of separated Tcell subsets. In CD7 ÿ cells no CD7 mRNA was monitored, indicating transcriptional regulation of CD7 expression. Certain differentiation-related antigens, including the cutaneous lymphocyte antigen CLA, were preferentially expressed on CD7 ÿ T cells. We suggest that absence of CD7 expression in a subset of CD4 memory cells reflects a separate and stable differentiation state occurring late in the immune response. These T cells may represent the physiological counterpart of malignant T cells in certain forms of cutaneous T-cell lymphoma.

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Anti‐CD2 (sheep red blood cell receptor) monoclonal antibodies and T cell activation I. Pairs of anti‐T11.1 and T11.2 (CD2 subgroups) are strongly mitogenic for T cells in presence of 12‐O‐tetradecanoylphorbol 13‐acetate

Cited by 76 publications

References 20 publications

Selection and characterization of T-cell variants lacking molecules involved in T-cell activation (T3 T-cell receptor, T44, and T11): analysis of the functional relationship among different pathways of activation.

Selection and characterization of T-cell variants lacking molecules involved in T-cell activation (T3 T-cell receptor, T44, and T11): analysis of the functional relationship among different pathways of activation.

Engagement of specific T-cell surface molecules regulates cytoskeletal polarization in HTLV-1–infected lymphocytes

CD7‐negative T cells represent a separate differentiation pathway in a subset of post‐thymic helper T cells

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