TY - JOUR
T1 - Effects of IL-4 and Fcγ receptor II engagement on Egr-1 expression during stimulation of B lymphocytes by membrane immunoglobulin crosslinking
AU - Klaus, Stephen J.
AU - Phillips, Nancy E.
AU - Parker, David C.
N1 - Funding Information:
Acknowledgements--We thank Dr John G. Monroe for providing the Egr-1 cDNA. This work was supported by American Cancer Society grants IM-327 (D.C.P.) and IM-447 (N.E.P.) and U.S.P.H.S. grant ROI-AI-24303. N.E.P. was the recipient of an Arthritis Foundation Investigator Award.
PY - 1993/11
Y1 - 1993/11
N2 - Egr-1 is an immediate early gene that is rapidly upregulated in response to mitogenic signals induced by antigen receptor crosslinking on murine B lymphocytes. It has been shown that levels of Egr-1 expression are closely correlated with B cell proliferation in several models of B cell activation and tolerance. We compared the expression of Egr-1 during B cell stimulation with Fab′2 and IgG anti-immunoglobulin (anti-IG), since it is known that Fab′2 anti-Ig is mitogenic while IgG anti-Ig is not, owing to a dominant inhibitory effect of crosslinking the B cell Fcγ RII to membrane Ig. While mitogenic doses of Fab′2 anti-Ig induce large and rapid increases in Egr-1 expression, IgG anti-Ig results in smaller increases in Egr-1 mRNA, comparable to that seen with submitogenic concentrations of Fab′2 anti-Ig. However, the correlation between Egr-1 expression and B cell proliferation breaks down when IL-4 is added as a co-mitogen to induce B cell proliferation with IgG anti-Ig or submitogenic concentrations of Fab′2 anti-Ig. No corresponding increases in Egr-1 mRNA levels are observed when IL-4 is added. Therefore, IL-4 overcomes Fc receptor-mediated inhibition of B cell proliferation without affecting inhibition of Egr-1 mRNA induction, as demonstrated earlier for c-myc mRNA in this system.
AB - Egr-1 is an immediate early gene that is rapidly upregulated in response to mitogenic signals induced by antigen receptor crosslinking on murine B lymphocytes. It has been shown that levels of Egr-1 expression are closely correlated with B cell proliferation in several models of B cell activation and tolerance. We compared the expression of Egr-1 during B cell stimulation with Fab′2 and IgG anti-immunoglobulin (anti-IG), since it is known that Fab′2 anti-Ig is mitogenic while IgG anti-Ig is not, owing to a dominant inhibitory effect of crosslinking the B cell Fcγ RII to membrane Ig. While mitogenic doses of Fab′2 anti-Ig induce large and rapid increases in Egr-1 expression, IgG anti-Ig results in smaller increases in Egr-1 mRNA, comparable to that seen with submitogenic concentrations of Fab′2 anti-Ig. However, the correlation between Egr-1 expression and B cell proliferation breaks down when IL-4 is added as a co-mitogen to induce B cell proliferation with IgG anti-Ig or submitogenic concentrations of Fab′2 anti-Ig. No corresponding increases in Egr-1 mRNA levels are observed when IL-4 is added. Therefore, IL-4 overcomes Fc receptor-mediated inhibition of B cell proliferation without affecting inhibition of Egr-1 mRNA induction, as demonstrated earlier for c-myc mRNA in this system.
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U2 - 10.1016/0161-5890(93)90463-L
DO - 10.1016/0161-5890(93)90463-L
M3 - Article
C2 - 8232340
AN - SCOPUS:0027331624
SN - 0161-5890
VL - 30
SP - 1553
EP - 1558
JO - Molecular Immunology
JF - Molecular Immunology
IS - 16
ER -