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The Journal of Immunology, 2004, 172: 7246-7253.
Copyright © 2004 by The American Association of Immunologists

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 Specificity1

Seishi Kyoizumi2,*, Takaaki Ohara{dagger}, Yoichiro Kusunoki*, Tomonori Hayashi*, Kazuaki Koyama* and Naohiro Tsuyama{ddagger}

* Laboratory of Immunology, Department of Radiobiology/Molecular Epidemiology, Radiation Effects Research Foundation, Hiroshima, Japan; {dagger} Life Science Laboratories, Life Science RD Center, Kaneka Corp., Takasago, Japan; and {ddagger} Cellular Signal Analysis, Department of Bio-Signal Analysis, Applied Medical Engineering Science, Yamaguchi University Graduate School of Medicine, Ube City, Japan

We have used HSCA-2, an mAb that recognizes a sialic acid-dependent epitope on the low molecular mass (~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.




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