CD4+ suppressor cells inhibit the function of effector cells of experimental autoimmune encephalomyelitis through a mechanism involving transforming growth factor-beta - PubMed (original) (raw)

. 1991 Feb 15;146(4):1163-8.

Affiliations

PMID: 1671402

CD4+ suppressor cells inhibit the function of effector cells of experimental autoimmune encephalomyelitis through a mechanism involving transforming growth factor-beta

W J Karpus et al. J Immunol. 1991.

Abstract

Nylon wool adherent, CD4+ T cells from the spleens of rats that have recovered from experimental autoimmune encephalomyelitis (EAE) inhibit the in vitro production of IFN-gamma, but not IL-2, by effector cells of EAE when cocultured in the presence of myelin basic protein Ag. When anti-transforming growth factor-beta (TGF-beta) antibodies are added to the co-cultures, IFN-gamma production is restored to normal levels. Irrelevant control antibodies have no effect. The same pattern of response was obtained with cells incubated in serum-free medium. In other experiments, purified TGF-beta was added to cultures of effector cells in the presence of antigen. TGF-beta inhibited the production of IFN-gamma by these cells in a dose-dependent manner, but had no apparent inhibitory effect on IL-2 production. Finally, supernatants from cultures containing effector cells and CD4+ suppressor cells plus Ag contained measurable amounts of TGF-beta, whereas supernatants from cultures of effector cells plus Ag contained no measurable amounts of TGF-beta. These results suggest that CD4+ Ts cells of EAE regulate effector cells of EAE through a mechanism that involves the secretion of TGF-beta and that the inhibitory function of this cytokine can be reversed with neutralizing antibodies directed against TGF-beta.

PubMed Disclaimer

Cited by

Augmentation of regulatory B cell activity in experimental allergic encephalomyelitis by glatiramer acetate.
Begum-Haque S, Christy M, Ochoa-Reparaz J, Nowak EC, Mielcarz D, Haque A, Kasper LH. Begum-Haque S, et al. J Neuroimmunol. 2011 Mar;232(1-2):136-44. doi: 10.1016/j.jneuroim.2010.10.031. Epub 2010 Nov 26. J Neuroimmunol. 2011. PMID: 21111489 Free PMC article.
Interleukin-12 induces relapse in experimental allergic encephalomyelitis in the Lewis rat.
Smith T, Hewson AK, Kingsley CI, Leonard JP, Cuzner ML. Smith T, et al. Am J Pathol. 1997 Jun;150(6):1909-17. Am J Pathol. 1997. PMID: 9176384 Free PMC article.
Both CD4+ and CD8+ T cells are essential to induce experimental autoimmune myasthenia gravis.
Zhang GX, Xiao BG, Bakhiet M, van der Meide P, Wigzell H, Link H, Olsson T. Zhang GX, et al. J Exp Med. 1996 Aug 1;184(2):349-56. doi: 10.1084/jem.184.2.349. J Exp Med. 1996. PMID: 8760788 Free PMC article.
Mechanisms of action of interferon-beta in multiple sclerosis.
Arnason BG, Dayal A, Qu ZX, Jensen MA, Genç K, Reder AT. Arnason BG, et al. Springer Semin Immunopathol. 1996;18(1):125-48. doi: 10.1007/BF00792613. Springer Semin Immunopathol. 1996. PMID: 8984676 Review. No abstract available.

CD4+ suppressor cells inhibit the function of effector cells of experimental autoimmune encephalomyelitis through a mechanism involving transforming growth factor-beta - PubMed (original) (raw)