|
|
||||||||
The Journal of Immunology, Vol 146, Issue 7 2176-2184, Copyright © 1991 by American Association of Immunologists
ARTICLES |
Y Torimoto, K Sugita, DS Weinberg, NH Dang, C Donahue, NL Letvin, SF Schlossman and C Morimoto
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.
We have developed a mAb anti-6C2, by immunizing mice with T cell line derived from the Callithrix jacchus (common marmoset). Anti-6C2 is reactive with approximately 50% of unfractionated T cells, 50% of CD4+ cells, and 40% of CD8+ cells. Regarding CD4+ cells, anti-6C2-reactive cells substantially overlap with the CD29+CD45RO+ Th cell population. Moreover, anti-6C2 can divide these T cells into 6C2+ and 6C2- subpopulations. The CD4+CD45RO+6C2+ cells maximally respond to soluble Ag such as tetanus toxoid and provide strong helper function for PWM- driven B cell IgG synthesis. Most interestingly, anti-6C2 was also reactive against activated B cells but not resting B cells; furthermore, this epitope was inducible through activation of resting B cells or B cell line. Biochemical characterization showed that anti-6C2 precipitated two glycoproteins with the relative molecular weights of 180,000 and 95,000 from 125I-surface labeled cell lysate. Sequential immunoprecipitation studies demonstrated that these two glycoproteins were the lymphocyte function-associated antigen (LFA-1) Ag complex (CD11a/18). Significantly, although this antibody did not inhibit cytotoxic killer T cell responses and Ag-induced T cell proliferation as did conventional anti-LFA-1, it did inhibit PWM-driven B cell IgG synthesis. Because 6C2 expression was induced after B cell activation, the above results strongly suggest that the 6C2 molecule may play a role in the interaction of CD4 helper cells and activated B lymphocytes.
This article has been cited by other articles:
![]() |
R. Mukasa, T. Homma, T. Ohtsuki, O. Hosono, A. Souta, T. Kitamura, M. Fukuda, S. Watanabe, and C. Morimoto Core 2-containing O-glycans on CD43 are preferentially expressed in the memory subset of human CD4 T cells Int. Immunol., February 1, 1999; 11(2): 259 - 268. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |