Differential transmembrane signaling in B lymphocyte activation

J. C. Cambier, Z. Z. Chen, J. T. Ransom, K. M. Coggeshall, Michael Klemsz, L. K. Harris, V. M. Sandoval, M. K. Newell

Research output: Contribution to journalArticle

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Abstract

In conclusion, we have discussed three physiologic stimulus-response systems operative in regulation of normal G(O) B lymphocyte function. Clearly transmembrane signal transduction by these receptors occurs by quite distinct mechanisms. Once bound by ligand, membrane IgM and IgD activate a PtdInsP2 hydrolysis cascade. BSF1 receptors do not use this mechanism, although surprisingly they activate I-A gene expression more efficiently than mIg-binding ligands. Finally, when bound by soluble ligands, I-A and I-E transduce negative signals that lead to suppression of anti-Ig responses. Transduction of this signal appears not to involve PtdIns metabolism but has a pronounced effect on PKC(a), lessening activatable cytosolic activity. The molecular basis of this effect is totally obscure. This report serves to illustrate the probable existence of multiple molecular pathways for transmembrane signaling beyond the defined α1-, α2- and β-adrenergic mechanisms. Further, they illustrate that the ultimate biologic response of cells may in many instances be a function of interactive aspects of the signaling machinery.

Original languageEnglish (US)
Pages (from-to)52-64
Number of pages13
JournalAnnals of the New York Academy of Sciences
Volume494
StatePublished - 1987
Externally publishedYes

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Lymphocytes
Lymphocyte Activation
B-Lymphocytes
Chemical activation
Ligands
Signal Transduction
Phosphatidylinositol 4,5-Diphosphate
Immunoglobulin D
Signal transduction
Phosphatidylinositols
Metabolism
Gene expression
Adrenergic Agents
Machinery
Immunoglobulin M
Hydrolysis
Membranes
Gene Expression
Activation
Transduction

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Cambier, J. C., Chen, Z. Z., Ransom, J. T., Coggeshall, K. M., Klemsz, M., Harris, L. K., ... Newell, M. K. (1987). Differential transmembrane signaling in B lymphocyte activation. Annals of the New York Academy of Sciences, 494, 52-64.

Differential transmembrane signaling in B lymphocyte activation. / Cambier, J. C.; Chen, Z. Z.; Ransom, J. T.; Coggeshall, K. M.; Klemsz, Michael; Harris, L. K.; Sandoval, V. M.; Newell, M. K.

In: Annals of the New York Academy of Sciences, Vol. 494, 1987, p. 52-64.

Research output: Contribution to journalArticle

Cambier, JC, Chen, ZZ, Ransom, JT, Coggeshall, KM, Klemsz, M, Harris, LK, Sandoval, VM & Newell, MK 1987, 'Differential transmembrane signaling in B lymphocyte activation', Annals of the New York Academy of Sciences, vol. 494, pp. 52-64.
Cambier JC, Chen ZZ, Ransom JT, Coggeshall KM, Klemsz M, Harris LK et al. Differential transmembrane signaling in B lymphocyte activation. Annals of the New York Academy of Sciences. 1987;494:52-64.
Cambier, J. C. ; Chen, Z. Z. ; Ransom, J. T. ; Coggeshall, K. M. ; Klemsz, Michael ; Harris, L. K. ; Sandoval, V. M. ; Newell, M. K. / Differential transmembrane signaling in B lymphocyte activation. In: Annals of the New York Academy of Sciences. 1987 ; Vol. 494. pp. 52-64.
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AB - In conclusion, we have discussed three physiologic stimulus-response systems operative in regulation of normal G(O) B lymphocyte function. Clearly transmembrane signal transduction by these receptors occurs by quite distinct mechanisms. Once bound by ligand, membrane IgM and IgD activate a PtdInsP2 hydrolysis cascade. BSF1 receptors do not use this mechanism, although surprisingly they activate I-A gene expression more efficiently than mIg-binding ligands. Finally, when bound by soluble ligands, I-A and I-E transduce negative signals that lead to suppression of anti-Ig responses. Transduction of this signal appears not to involve PtdIns metabolism but has a pronounced effect on PKC(a), lessening activatable cytosolic activity. The molecular basis of this effect is totally obscure. This report serves to illustrate the probable existence of multiple molecular pathways for transmembrane signaling beyond the defined α1-, α2- and β-adrenergic mechanisms. Further, they illustrate that the ultimate biologic response of cells may in many instances be a function of interactive aspects of the signaling machinery.

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