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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yoshikawa, H. Articles by Tasaka, K. Search for Related Content PubMed PubMed Citation Articles by Yoshikawa, H. Articles by Tasaka, K. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  FcRIII-Mediated Regulation of Hematopoiesis in Murine Bone Marrow Cells by Interleukin-3 and CD95 (Fas/Apo-1) Hideshi Yoshikawa, Toshiko Sakihama, Yasuo Nakajima, and Kachio Tasaka From the Department of Parasitology and Immunology, Yamanashi Medical University, Yamanashi, Japan. The interleukin-3 (IL-3)-dependent murine bone marrow-derived cell line FDC-P2/185-4 (185-4) undergoes apoptosis when IL-3 is withdrawn from culture medium. Previous results from our studies indicated that a high concentration of aggregated mouse IgG prevented apoptosis of 185-4 cells through FcRIII by an autocrine mechanism, producing IL-3. But after 24 hours, 185-4 cells expressed CD95 (Fas/Apo-1) on their surfaces on stimulation via FcRIII. In addition, this CD95 was functional and apoptosis was induced by anti-CD95 monoclonal antibody (MoAb). We investigated how these conflicting effects were induced by FcRIII stimulation within the context of cell survival and death. The results showed that IL-3 was induced by calcium ionophore and that the IL-3 induced by FcRIII stimulation was blocked by EGTA or FK506, but not by staurosporine (protein kinase C [PKC] inhibitor), indicating the important role of calcium-calcineurin in this system. On the other hand, the CD95 expression induced by FcRIII stimulation was blocked by staurosporine, but not by EGTA or FK506, and phorbol myristate acetate (PMA) induced CD95 expression in the same manner as FcRIII, indicating the involvement of PKC in the CD95 expression induced by FcRIII stimulation. Thus, FcRIII-mediated stimulation even while promoting immediate survival of the bone marrow cells, also triggers mechanisms that will facilitate their eventual deletion at the end of the response. These results suggest that a balance between cell survival and death is maintained to avoid unlimited cell growth caused by FcRIII-ligand interaction in hematopoiesis during inflammation. Blood, Vol. 90 No. 5 (September 1), 1997: pp. 1911-1919 © 1997 by The American Society of Hematology. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Yoshikawa, Y. Nakajima, and K. Tasaka Enhanced Expression of Fas-Associated Death Domain-Like IL-1-Converting Enzyme (FLICE)-Inhibitory Protein Induces Resistance to Fas-Mediated Apoptosis in Activated Mast Cells J. Immunol., December 1, 2000; 165(11): 6262 - 6269. [Abstract] [Full Text] [PDF] H. Yoshikawa, Y. Nakajima, and K. Tasaka Glucocorticoid Suppresses Autocrine Survival of Mast Cells by Inhibiting IL-4 Production and ICAM-1 Expression J. Immunol., May 15, 1999; 162(10): 6162 - 6170. [Abstract] [Full Text] [PDF]

	Copyright © 1997 by American Society of Hematology         Online ISSN: 1528-0020