Skip to main content
The Journal of Experimental Medicine logoLink to The Journal of Experimental Medicine
. 1993 Mar 1;177(3):857–861. doi: 10.1084/jem.177.3.857

Abnormal transcription factor induction through the surface immunoglobulin M receptor of B-1 lymphocytes

PMCID: PMC2190944  PMID: 8436914

Abstract

Populations of murine peritoneal B-1 and splenic B-2 cells, highly purified by negative selection techniques, were used to demonstrate that B-1 cells completely fail to enter cell cycle in response to surface immunoglobulin M (sIgM) crosslinking without any decrease in cell number or viability. This failure of B-1 cell responsiveness appears to represent a specific defect in sIgM-derived signaling inasmuch as stimulation to enter S phase occurs normally in response to activated and fixed T cells, and to lipopolysaccharide (LPS). The level at which sIgM signaling fails was determined by evaluating the nuclear expression of the transcription factor complex, NF-kappa B, whose sIgM- mediated induction in B-2 cells is dependent on protein kinase C (PKC) activation but is independent of protein synthesis. There was no induction of nuclear NF-kappa B in B-1 cells stimulated by sIgM crosslinking, although NF-kappa B was stimulated by phorbol myristate acetate and by LPS. In contrast, NF-kappa B was induced in B-2 cells by all three stimuli. Thus, in B-1 cells, the sIgM-mediated induction of a transcription factor that is substantially stimulated by anti-IgM in B- 2 cells is blocked. However, all sIgM-derived signaling in B-1 cells was not impaired inasmuch as anti-IgM increased I-A antigen expression. These results strongly suggest that sIgM receptor-mediated signaling in B-1 cells is interrupted early in the signal transduction pathway, at a point proximal to the activation of PKC. These results further demonstrate that transcription factor induction can be used to analyze the level at which receptor-mediated signaling is blocked.

Full Text

The Full Text of this article is available as a PDF (854.4 KB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Cohen D. P., Rothstein T. L. Elevated levels of protein kinase C activity and alpha-isoenzyme expression in murine peritoneal B cells. J Immunol. 1991 May 1;146(9):2921–2927. [PubMed] [Google Scholar]
  2. Cong Y. Z., Rabin E., Wortis H. H. Treatment of murine CD5- B cells with anti-Ig, but not LPS, induces surface CD5: two B-cell activation pathways. Int Immunol. 1991 May;3(5):467–476. doi: 10.1093/intimm/3.5.467. [DOI] [PubMed] [Google Scholar]
  3. Ghosh S., Baltimore D. Activation in vitro of NF-kappa B by phosphorylation of its inhibitor I kappa B. Nature. 1990 Apr 12;344(6267):678–682. doi: 10.1038/344678a0. [DOI] [PubMed] [Google Scholar]
  4. Kawakami K., Parker D. C. Differences between T helper cell type I (Th1) and Th2 cell lines in signalling pathways for induction of contact-dependent T cell help. Eur J Immunol. 1992 Jan;22(1):85–93. doi: 10.1002/eji.1830220114. [DOI] [PubMed] [Google Scholar]
  5. Kipps T. J. The CD5 B cell. Adv Immunol. 1989;47:117–185. doi: 10.1016/s0065-2776(08)60663-x. [DOI] [PubMed] [Google Scholar]
  6. Kolber D. L., Shultz L. D., Rothstein T. L. Phorbol ester responsiveness of murine Ly-1-lineage B cells from normal and viable motheaten mutant mice. Eur J Immunol. 1991 Mar;21(3):721–729. doi: 10.1002/eji.1830210327. [DOI] [PubMed] [Google Scholar]
  7. Liou L. B., Warner G. L., Scott D. W. Can peritoneal B cells be rendered unresponsive? Int Immunol. 1992 Jan;4(1):15–21. doi: 10.1093/intimm/4.1.15. [DOI] [PubMed] [Google Scholar]
  8. Liu J. L., Chiles T. C., Sen R. J., Rothstein T. L. Inducible nuclear expression of NF-kappa B in primary B cells stimulated through the surface Ig receptor. J Immunol. 1991 Mar 1;146(5):1685–1691. [PubMed] [Google Scholar]
  9. Murphy T. P., Kolber D. L., Rothstein T. L. Elevated expression of Pgp-1 (Ly-24) by murine peritoneal B lymphocytes. Eur J Immunol. 1990 May;20(5):1137–1142. doi: 10.1002/eji.1830200529. [DOI] [PubMed] [Google Scholar]
  10. Noelle R. J., Roy M., Shepherd D. M., Stamenkovic I., Ledbetter J. A., Aruffo A. A 39-kDa protein on activated helper T cells binds CD40 and transduces the signal for cognate activation of B cells. Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6550–6554. doi: 10.1073/pnas.89.14.6550. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. O'Garra A., Howard M. Cytokines and Ly-1 (B1) B cells. Int Rev Immunol. 1992;8(2-3):219–234. doi: 10.3109/08830189209055575. [DOI] [PubMed] [Google Scholar]
  12. Plater-Zyberk C., Brown C. M., Andrew E. M., Maini R. N. CD5+B in rheumatoid arthritis. Ann N Y Acad Sci. 1992 May 4;651:540–550. doi: 10.1111/j.1749-6632.1992.tb24660.x. [DOI] [PubMed] [Google Scholar]
  13. Rooney J. W., Dubois P. M., Sibley C. H. Cross-linking of surface IgM activates NF-kappa B in B lymphocyte. Eur J Immunol. 1991 Dec;21(12):2993–2998. doi: 10.1002/eji.1830211214. [DOI] [PubMed] [Google Scholar]
  14. Rothstein T. L., Kolber D. L. Anti-Ig antibody inhibits the phorbol ester-induced stimulation of peritoneal B cells. J Immunol. 1988 Dec 15;141(12):4089–4093. [PubMed] [Google Scholar]
  15. Rothstein T. L., Kolber D. L. Peritoneal B cells respond to phorbol esters in the absence of co-mitogen. J Immunol. 1988 May 1;140(9):2880–2885. [PubMed] [Google Scholar]
  16. Rothstein T. L. Polyreactive low-affinity IgM antibodies produced by CD5+ B cells. Immunol Today. 1990 May;11(5):152–152. doi: 10.1016/0167-5699(90)90062-e. [DOI] [PubMed] [Google Scholar]

Articles from The Journal of Experimental Medicine are provided here courtesy of The Rockefeller University Press

RESOURCES