Expression characteristics and stimulatory functions of CD43 in human CD4+ memory T cells: analysis using a monoclonal antibody to CD43 that has a novel lineage specificity |
| |
Authors: | Kyoizumi Seishi Ohara Takaaki Kusunoki Yoichiro Hayashi Tomonori Koyama Kazuaki Tsuyama Naohiro |
| |
Affiliation: | Laboratory of Immunology, Department of Radiobiology/Molecular Epidemiology, Radiation Effects Research Foundation, 5-2 Hijiyama Park, Minami Ward, Hiroshima 732-0815, Japan. kyoizumi@rerf.or.jp |
| |
Abstract: | We have used HSCA-2, an mAb that recognizes a sialic acid-dependent epitope on the low molecular mass (approximately 115-kDa) glycoform of CD43 that is expressed in resting T and NK cells, to examine the expression characteristics and stimulatory functions of CD43 in human CD4+ memory T cells. Having previously reported that the memory cells that respond to recall Ags in a CD4+ CD45RO+ T cell population almost all belong to a subset whose surface CD43 expression levels are elevated, we now find that exposing these same memory T cells to HSCA-2 mAb markedly increases their proliferative responsiveness to recall Ags. We think it unlikely that this increase in responsiveness is a result of CD43-mediated monocyte activation, especially given that the HSCA-2 mAb differs from all previously used CD43 mAbs in having no obvious binding specificity for monocyte CD43. Predictably, treatment with HSCA-2 mAb did not lead to significant recall responses in CD4+ CD45RO+ T cells, whose CD43 expression levels were similar to or lower than those of naive cells. Other experiments indicated that the HSCA-2 mAb was capable of enhancing the proliferative responsiveness of CD4+ memory T cells that had been exposed to polyclonal stimulation by monocyte-bound CD3 mAb and could also act in synergy with CD28 mAb to enhance the responsiveness of CD4+ T cells to CD3 stimulation. Taken together, these findings suggest that the CD43 molecules expressed on CD4+ memory T cells may be capable of enhancing the costimulatory signaling and hence providing accessory functions to TCR-mediated activation processes. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|