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Transforming growth factor beta is an important immunomodulatory protein for human B lymphocytes.
Abstract
The growth and differentiation of B cells to immunoglobulin (Ig)-secreting cells is regulated by a variety of soluble factors. This study presents data that support a role for transforming growth factor (TGF)-beta in this regulatory process. B lymphocytes were shown to have high-affinity receptors for TGF-beta that were increased fivefold to sixfold after in vitro activation. The addition of picogram quantities of TGF-beta to B cell cultures suppressed factor-dependent, interleukin 2 (IL 2) B cell proliferation and markedly suppressed factor-dependent (IL 2 or B cell differentiation factor) B cell Ig secretion. In contrast, the constitutive IgG production by an Epstein Barr virus-transformed B cell line was not modified by the presence of TGF-beta in culture. This cell line was found to lack high-affinity TGF-beta receptors. The degree of inhibition of B cell proliferation observed in in vitro cultures was found to be dependent not only on the concentration of TGF-beta added but also on the concentration of the growth stimulatory substance (IL 2) present. By increasing the IL 2 concentrations in culture, the inhibition of proliferation induced by TGF-beta could be partially overcome. In contrast, the inhibition of Ig secretion induced by TGF-beta could not be overcome by a higher concentration of stimulatory factor, demonstrating that the suppression of B cell differentiation by TGF-beta is not due solely to its effects on proliferation. Furthermore, it was demonstrated that B lymphocytes secrete TGF-beta. Unactivated tonsillar B cells had detectable amounts of TGF-beta mRNA on Northern blot analysis, and B cell activation with Staphylococcus aureus Cowan (SAC) resulted in a twofold to threefold increase in TGF-beta mRNA. Supernatants conditioned by unactivated B cells had small amounts of TGF-beta, SAC activation of the B cells resulted in a sixfold to sevenfold increase in the amount of TGF-beta present in the supernatants. Thus, B lymphocytes synthesize and secrete TGF-beta and express receptors for TGF-beta. The addition of exogenous TGF-beta to cultures of stimulated B cells inhibits subsequent proliferation and Ig secretion. TGF-beta may function as an autocrine growth inhibitor that limits B lymphocyte proliferation and ultimate differentiation.
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Citations
Cited by
Shull, M. M., Ormsby, I., Kier, A. B., Pawlowski, S., Diebold, R. J., Yin, M., Allen, R., Sidman, C., Proetzel, G., Calvin, D., et al. (1992) · Nature · doi:10.1038/359693a0 · Cited by 2,985
TGF-β Signaling in Tumor Suppression and Cancer Progression
Derynck, R., Akhurst, R. J., & Balmain, A. (2001) · Nature Genetics · doi:10.1038/ng1001-117 · Cited by 2,275
Growth inhibition by TGF-β linked to suppression of retinoblastoma protein phosphorylation.
Laiho, M., DeCaprio, J. A., Ludlow, J. W., Livingston, D. M., & Massague, J. (1990) · Cell · doi:10.1016/0092-8674(90)90251-9 · Cited by 797
Transforming Growth Factor‐β: Major Role in Regulation of Extracellular Matrix
ROBERTS, A. B., HEINE, U. I., FLANDERS, K. C., & SPORN, M. B. (1990) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1990.tb17931.x · Cited by 696
Self-citationDefrance, T., Vanbervliet, B., Brière, F., Durand, I., Rousset, F., & Banchereau, J. (1992) · The Journal of experimental medicine · doi:10.1084/jem.175.3.671 · Cited by 638
Metadata
- Authors
- Kehrl, J. H., Roberts, A. B., Wakefield, L. M., Jakowlew, S., Sporn, M. B., & Fauci, A. S.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1986-12
- Volume
- 137
- Issue
- 12
- Pages
- 3855-3860
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1594069877
- Cited by
- 759
- References
- 0
- FWCI
- 14.00
- Type
- journal article
- Language
- en
- Open access
- closed
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- Kehrl, J. H., Roberts, A. B., Wakefield, L. M., Jakowlew, S., Sporn, M. B., & Fauci, A. S. (1986). Transforming growth factor beta is an important immunomodulatory protein for human B lymphocytes. The Journal of Immunology. https://doi.org/10.4049/jimmunol.137.12.3855
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