The suppressive effect of TGF-beta on IL-12-mediated immune modulation specific to a peptide Ac1-11 of myelin basic protein (MBP): a mechanism involved in inhibition of both IL-12 receptor beta1 and beta2.
Publication/Presentation Date
8-1-2000
Abstract
Transforming growth factor (TGF)-beta exerts a counter-regulatory effect on interleukin (IL)-12-mediated immune modulation. The underlying mechanism is not fully understood. Here we demonstrate that the expression of IL-12Rbeta1 and IL-12Rbeta2 in MBP peptide Ac1-11-primed splenocytes is upregulated upon antigen stimulation. TGF-beta induces an unresponsiveness of these primed splenocytes to IL-12 signaling through a mechanism involved in inhibition of both IL-12Rbeta1 and beta2. The modulation of IL-12Rbeta1 and beta2 expression by Ac1-11 stimulation and TGF-beta is mainly involved in CD4+ population. These data indicate that both IL-12Rbeta1 and IL-12Rbeta2 expression are crucial during T cell activation. TGF-beta-induced inhibition of IL-12R expression will reduce cellular immune responses during IL-12-mediated autoimmune disease.
Volume
108
Issue
1-2
First Page
53
Last Page
63
ISSN
0165-5728
Published In/Presented At
Xu, H., Zhang, G. X., Wysocka, M., Wu, C. Y., Trinchieri, G., & Rostami, A. (2000). The suppressive effect of TGF-beta on IL-12-mediated immune modulation specific to a peptide Ac1-11 of myelin basic protein (MBP): a mechanism involved in inhibition of both IL-12 receptor beta1 and beta2. Journal of neuroimmunology, 108(1-2), 53–63. https://doi.org/10.1016/s0165-5728(00)00278-2
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
10900337
Department(s)
Administration and Leadership
Document Type
Article