Tags

Type your tag names separated by a space and hit enter

Immunoregulation of encephalitogenic MBP-NAc1-11-reactive T cells by CD4+ TCR-specific T cells involves IL-4, IL-10 and IFN-gamma.
Autoimmunity 1999; 31(4):237-48A

Abstract

The generation of TCR transgenic (Tg) mice expressing a BV8S2 (Vbeta8 subfamily 2) chain specific for the encephalitogenic NAc1-11 region of MBP provides a unique system for evaluating the mechanisms involved in anti-TCR immunoregulation of EAE. In a previous study, we showed that vaccination with BV8S2 protein induced specific T cells that inhibited proliferation responses and encephalitogenic activity of MBP-reactive T cells in vitro, and resulted in a skewed production of Th2 cytokines by the MBP-reactive T cells. These data suggested that regulation of the encephalitogenic T cells was mediated by inhibitory cytokines rather than through a deletional mechanism. In the current study, we have employed the BV8S2 Tg mouse model to address the issue of which cytokines produced by anti-TCR-reactive T cells can regulate the function of encephalitogenic Th1 cells. Utilizing neutralizing anti-cytokine antibodies to reverse inhibitory effects of supernatants from BV8S2-specific T cells, we found that IL-4, IL-10, and to a lesser extent, IFN-gamma and TGF-beta, were the major regulatory cytokines responsible for inhibiting encephalitogenic activity, proliferation, and IFN-gamma secretion of MBP-NAc1-11-reactive Th1 cells. These results indicate that cytokine regulation is the major mechanism through which TCR specific CD4+ T cells regulate encephalitogenic and potentially other bystander Th1 cells.

Authors+Show Affiliations

Neuroimmunology Research, R&D-31, Veterans Affairs Medical Center, Portland, OR 97201, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10789989

Citation

Adlard, K, et al. "Immunoregulation of Encephalitogenic MBP-NAc1-11-reactive T Cells By CD4+ TCR-specific T Cells Involves IL-4, IL-10 and IFN-gamma." Autoimmunity, vol. 31, no. 4, 1999, pp. 237-48.
Adlard K, Tsaknardis L, Beam A, et al. Immunoregulation of encephalitogenic MBP-NAc1-11-reactive T cells by CD4+ TCR-specific T cells involves IL-4, IL-10 and IFN-gamma. Autoimmunity. 1999;31(4):237-48.
Adlard, K., Tsaknardis, L., Beam, A., Bebo, B. F., Vandenbark, A. A., & Offner, H. (1999). Immunoregulation of encephalitogenic MBP-NAc1-11-reactive T cells by CD4+ TCR-specific T cells involves IL-4, IL-10 and IFN-gamma. Autoimmunity, 31(4), pp. 237-48.
Adlard K, et al. Immunoregulation of Encephalitogenic MBP-NAc1-11-reactive T Cells By CD4+ TCR-specific T Cells Involves IL-4, IL-10 and IFN-gamma. Autoimmunity. 1999;31(4):237-48. PubMed PMID: 10789989.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immunoregulation of encephalitogenic MBP-NAc1-11-reactive T cells by CD4+ TCR-specific T cells involves IL-4, IL-10 and IFN-gamma. AU - Adlard,K, AU - Tsaknardis,L, AU - Beam,A, AU - Bebo,B F,Jr AU - Vandenbark,A A, AU - Offner,H, PY - 2000/5/2/pubmed PY - 2000/5/20/medline PY - 2000/5/2/entrez SP - 237 EP - 48 JF - Autoimmunity JO - Autoimmunity VL - 31 IS - 4 N2 - The generation of TCR transgenic (Tg) mice expressing a BV8S2 (Vbeta8 subfamily 2) chain specific for the encephalitogenic NAc1-11 region of MBP provides a unique system for evaluating the mechanisms involved in anti-TCR immunoregulation of EAE. In a previous study, we showed that vaccination with BV8S2 protein induced specific T cells that inhibited proliferation responses and encephalitogenic activity of MBP-reactive T cells in vitro, and resulted in a skewed production of Th2 cytokines by the MBP-reactive T cells. These data suggested that regulation of the encephalitogenic T cells was mediated by inhibitory cytokines rather than through a deletional mechanism. In the current study, we have employed the BV8S2 Tg mouse model to address the issue of which cytokines produced by anti-TCR-reactive T cells can regulate the function of encephalitogenic Th1 cells. Utilizing neutralizing anti-cytokine antibodies to reverse inhibitory effects of supernatants from BV8S2-specific T cells, we found that IL-4, IL-10, and to a lesser extent, IFN-gamma and TGF-beta, were the major regulatory cytokines responsible for inhibiting encephalitogenic activity, proliferation, and IFN-gamma secretion of MBP-NAc1-11-reactive Th1 cells. These results indicate that cytokine regulation is the major mechanism through which TCR specific CD4+ T cells regulate encephalitogenic and potentially other bystander Th1 cells. SN - 0891-6934 UR - https://www.unboundmedicine.com/medline/citation/10789989/Immunoregulation_of_encephalitogenic_MBP_NAc1_11_reactive_T_cells_by_CD4+_TCR_specific_T_cells_involves_IL_4_IL_10_and_IFN_gamma_ L2 - http://www.tandfonline.com/doi/full/10.3109/08916939908994069 DB - PRIME DP - Unbound Medicine ER -