CR2 ligands modulate human B cell activation.
A considerable body of evidence from this and other laboratories indicates that complement receptor type 2 (CR2) modulates B cell activation and growth. In the present studies we have examined the effects of three different types of CR2 ligands, i.e., monomeric, aggregated, and latex-bound C3dg; mAb to different CR2 epitopes; and UV-inactivated, non-transforming EBV (EBVUV) for their actions on highly purified, high density resting tonsil B cells. Although none of these ligands induced B cells to enter the cell cycle or synergized with either anti-mu or low m.w. B cell growth factor in triggering B cell mitogenesis, aggregated C3dg, latex-bound C3dg, the OKB7 anti-CR2 mAb, and EBVUV-enhanced thymidine incorporation by phorbol ester-activated tonsil B cells. Such enhancement was not T cell or monocyte dependent. The major action of the CR2 ligands thus seems to be to enhance the transition of B cells activated by certain stimuli from the G1 to the S phase of the cell cycle. In contrast to the action of aggregated and latex-bound C3dg, monomeric C3dg was inhibitory for phorbol ester and aggregated C3dg-induced B cell activation. The HB-5 anti-CR2 mAb, which reacts with a different epitope on CR2 from that of OKB7, did not synergize with PMA in B cell activation. These data provide additional evidence for a role for the CR2 in the control of B cell growth and provide a useful model for studying the CR2-mediated signals that affect the growth of B cells.
Bohnsack
J F
JF
Department of Immunology, Scripps Clinic, La Jolla, CA 92037.
Cooper
N R
NR
D000276:Adjuvants, Immunologic / Q000502:physiology*; D000293:Adolescent; D000888:Antibodies, Anti-Idiotypic / Q000502:physiology; D000911:Antibodies, Monoclonal / Q000502:physiology; D000944:Antigens, Differentiation, B-Lymphocyte / Q000502:physiology*; D001402:B-Lymphocytes / Q000276:immunology*; D002453:Cell Cycle / Q000187:drug effects; D002648:Child; D002675:Child, Preschool; D003176:Complement C3 / Q000378:metabolism*; D004357:Drug Synergism; D000939:Epitopes / Q000276:immunology; D006801:Humans; D007075:Immunoglobulin M / Q000276:immunology / Q000502:physiology; D015847:Interleukin-4; D007378:Interleukins / Q000502:physiology*; D007399:Interphase / Q000187:drug effects; D008213:Lymphocyte Activation / Q000187:drug effects*; D009000:Monocytes / Q000276:immunology; D014066:Palatine Tonsil / Q000166:cytology; D011951:Receptors, Complement / Q000502:physiology*; D017464:Receptors, Complement 3d; D013601:T-Lymphocytes / Q000276:immunology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D000276:Adjuvants, Immunologic; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D000944:Antigens, Differentiation, B-Lymphocyte; D003176:Complement C3; D000939:Epitopes; D007075:Immunoglobulin M; D007378:Interleukins; D011951:Receptors, Complement; D017464:Receptors, Complement 3d; C044203:anti-IgM; D015847:Interleukin-4; D013755:Tetradecanoylphorbol Acetate