Previous studies have indicated that the murine surface antigen Lyb2 is involved in an activation pathway that apparently does not involve the surface immunoglobulin receptor. As sIg has been shown to transduce its activation signal through the breakdown of phosphatidylinositol (PI), and since activation via Lyb2 does not involve sIg, it was of interest to determine if binding to Lyb2 generates a PI response. We have demonstrated that an allele-specific monoclonal antibody to Lyb2 (anti-Lyb2 mab), which has previously been shown to drive B cells into S, also activated PI metabolism in these cells. This activation occurred in a dose-dependent and allelespecific manner. Antibodies to other B-cell surface molecules such as Ia did not induce a PI response. The effect of anti-Lyb2 mab was always less in magnitude than that induced by anti-IgM, but the effects of the two antibody preparations were most comparable in larger, presumptively preactivated cells. To explore the issue that Lyb2 may represent a receptor for a growth factor, possibly the early-acting B-cell growth factor BSF-1, we studied the PI response to BSF-1 and the effect of BSF-1 on Lyb2-induced PI turnover. BSF-1 neither induced a PI response nor inhibited competitively the response induced by anti-Lyb2 mab.
|Number of pages||9|
|State||Published - Nov 1987|
Bibliographical noteFunding Information:
We thank Ms. Joan Morris for her expert technical assistance and Drs. Alan Kaplan and E. C. Snow for their review ofthis manuscript. This project was supported by Grant HL27333 from the National Institutes of Health. S. A. Grupp was supported by NIH Training Grant HL07527; B. Subbarao was supported by NIH Grant AI21490 and appropriations from the Small Research Project Awards and the Tobacco and Health Research Institute of the University of Kentucky.
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