Induction of phorbol ester responsiveness in conventional B cells after activation via surface Ig

• Published in: The Journal of immunology (1950) Vol. 147; no. 11; pp. 3728 - 3735
• Main Authors: Rothstein, TL, Kolber, DL, Murphy, TP, Cohen, DP
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 01-12-1991; American Association of Immunologists
• Subjects: Animals; Antigens, CD - analysis; B-Lymphocytes - physiology; Biological and medical sciences; CD5 Antigens; Cell Cycle - drug effects; Cyclic AMP - physiology; Dose-Response Relationship, Drug; Dose-Response Relationship, Immunologic; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Immunobiology; Interleukin-4 - pharmacology; Lymphocyte Activation; Lymphoid cells: ontogeny, maturation, markers, receptors, circulation and recirculation; Mice; Mice, Inbred BALB C; Phorbol Esters - pharmacology; Protein Kinase C - physiology; Receptors, Antigen, B-Cell - physiology; Time Factors; Cell proliferation; Signal transduction; Vertebrata; Immunoglobulins; Signal; Mammalia; Mouse; Rodentia; Cell cycle; B-Lymphocyte; Mechanism of action; Cell surface
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.147.11.3728

The signals required to induce S phase entry in murine splenic B cells were found to be altered by prolonged treatment with low doses of anti-Ig antibody. Whereas fresh splenic B cells are stimulated by the combination of a phorbol ester protein kinase C agonist plus a calcium ionophore, anti-Ig-treated splenic B cells were stimulated by phorbol ester alone, in the absence of a comitogen. The majority of these phorbol ester responsive B cells expressed CD5. The phorbol ester responses of anti-Ig-treated splenic B cells paralleled those previously reported for untreated peritoneal CD5+ B cells in a number of respects: responses were not idiosyncratic to phorbol esters but occurred with nonphorbol protein kinase C agonists; phorbol ester responses were enhanced by IL-4; and, phorbol ester responses occurred rapidly and were greater at 24 than at 48 h. However, the effect of agents that act to raise intracellular levels of cAMP distinguished between anti-Ig-treated splenic B cells and untreated peritoneal B cells in that the phorbol ester responses of the former were enhanced whereas the responses of the latter were inhibited. The present results add a functional dimension to the phenotypic similarity between splenic B cells treated with anti-Ig and resident peritoneal B cells that constitutively express CD5; however, some differences in behavior were noted.