TY - JOUR
T1 - Amplification of suppressor inducer pathway with monoclonal antibody, anti-2H4, identifying a novel epitope of the common leukocyte antigen/T200 antigen
AU - Takeuchi, Tsutomu
AU - Rudd, Christopher E.
AU - Tedder, Thomas F.
AU - Schlossman, Stuart F.
AU - Morimoto, Chikao
N1 - Funding Information:
’ This work was supported by NIH Grants AI 12069, CA 25369, and AR 337 13. * Drs. T. Takeuchi and C. Rudd are recipients of postdoctoral fellowships from the Cancer Research Institute, New York. 3 Dr. T. Tedder is a research fellow of the Damon Runyon-Walter Winchell Cancer Fund, DRG-864. 4 To whom correspondence should be addressed at Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02 I 15. J Abbreviations used: AMLR, autologous mixed lymphocyte reaction; LCA, leukocyte common antigen; MHC, major histocompatibiiity complex; PBL, peripheral blood lymphocytes: PWM, pokeweed mitogen; Ig, immunoglobulin; RIA, radioimmunoassay; IL-2R; IL-2 receptor, FCS, fetal calf serum; CTL, cytotoxic T lymphocytes.
PY - 1989/1
Y1 - 1989/1
N2 - The 2H4 antigen, comprised of a 200 220-kDa glycoprotein of the leukocyte common antigen (LCA) family, is expressed on a suppressor inducer, but not a helper inducer subset of T4 cells. Earlier studies have demonstrated that the T4+2H4+ subset of cells maximally responded to the AMLR and this molecule had an important role in generated suppressor signals in AMLR/ Con A-activated T cell systems. In the present study, we examined the effect of a series of monoclonal antibodies including anti-2H4 antibody on the initial activation of T4 cells in response to self-Ia antigens. We found that the addition of anti-2H4 antibody resulted in an augmentation of the proliferative response of T4 cells in AMLR, whereas other antibodies reactive with LCA/ T200 antigens lacked this ability. Furthermore, anti-2H4 antibody enhanced both IL-2 production and IL-2R expression in this AMLR system. This enhancing effect was inhibited by anti-T3 antibody. Moreover, the suppressor inducer function of AMLR T4 cells was enhanced with anti-2H4 antibody by increasing the number of 2H4+ cells with high antigen density. Taken together, these results suggest that the 2H4 antigen may serve as an accessory structure for enhancing the activation of the T4+2H4+ suppressor inducer subset at initiation of cell triggering.
AB - The 2H4 antigen, comprised of a 200 220-kDa glycoprotein of the leukocyte common antigen (LCA) family, is expressed on a suppressor inducer, but not a helper inducer subset of T4 cells. Earlier studies have demonstrated that the T4+2H4+ subset of cells maximally responded to the AMLR and this molecule had an important role in generated suppressor signals in AMLR/ Con A-activated T cell systems. In the present study, we examined the effect of a series of monoclonal antibodies including anti-2H4 antibody on the initial activation of T4 cells in response to self-Ia antigens. We found that the addition of anti-2H4 antibody resulted in an augmentation of the proliferative response of T4 cells in AMLR, whereas other antibodies reactive with LCA/ T200 antigens lacked this ability. Furthermore, anti-2H4 antibody enhanced both IL-2 production and IL-2R expression in this AMLR system. This enhancing effect was inhibited by anti-T3 antibody. Moreover, the suppressor inducer function of AMLR T4 cells was enhanced with anti-2H4 antibody by increasing the number of 2H4+ cells with high antigen density. Taken together, these results suggest that the 2H4 antigen may serve as an accessory structure for enhancing the activation of the T4+2H4+ suppressor inducer subset at initiation of cell triggering.
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U2 - 10.1016/0008-8749(89)90358-4
DO - 10.1016/0008-8749(89)90358-4
M3 - Article
C2 - 2463098
AN - SCOPUS:0024537948
SN - 0008-8749
VL - 118
SP - 68
EP - 84
JO - Cellular Immunology
JF - Cellular Immunology
IS - 1
ER -