Staphylococcal enterotoxin B and tumor-necrosis factor-α-induced relapses of experimental allergic encephalomyelitis: Protection by transforming growth factor-β and interleukin-10

Giovanna M. Crisi, Laura Santambrogio, Gerald M. Hochwald, Sidney R. Smith, Joseph A. Carlino, G. Jeanette Thorbecke

Research output: Contribution to journalArticle

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Abstract

A study was made of the ability of the superantigen staphylococcal enterotoxin B (SEB) to induce relapses of experimental allergic encephalomyelitis (EAE) in SJL mice that had partially or completely recovered from acute EAE. We find that a single injection of 0.05 mg SEB i.v. induces mild relapses in 50% of such mice. In addition, tumor necrosis factor (TNF)-α (0.2 μg, i.p.) also induces EAE relapses in 43% of SJL mice when injected 1-2 months after recovery. SEB does not induce a second relapse if reinjected when Vβ17a+ T cells are still partially deleted. In these mice, however, TNF-α is equally effective in inducing relapses as in mice that did not receive SEB previously. We showed earlier that transforming growth factor (TGF)-β and TNF-α have antagonistic effects on experimental autoimmune diseases; e.g., in spontaneously relapsing EAE, TGF-β and anti-TNF were protective, while anti-TGF-β caused disease exacerbation. Interleukin (IL)-10 is also known to counteract certain TNF effects. We now find that both human IL-10 and TGF-β2 lower the incidence of EAE relapses when given simultaneously with SEB or TNF-α. The protective effect of TGF-β is significant only against relapses induced by SEB (reduced to 9%), and that of IL-10 only against relapses induced by TNF (reduced to 0%) with the treatment regimens employed. Neutralizing anti-TGF-β does not increase the incidence of SEB-induced EAE relapses. In contrast, anti-IL-10 increases both the incidence and the severity of such relapses. We conclude that TNF production is probably important in causing EAE relapses, but that other aspects of the SEB-induced reactivation of myelin-specific T cells also contribute. Furthermore, endogenous IL-10 rather than TGF-β production appears to limit the susceptibility to induction of EAE relapses in this model.

Original languageEnglish (US)
Pages (from-to)3035-3040
Number of pages6
JournalEuropean Journal of Immunology
Volume25
Issue number11
DOIs
StatePublished - Nov 1995
Externally publishedYes

Fingerprint

Autoimmune Experimental Encephalomyelitis
Transforming Growth Factors
Interleukin-10
Tumor Necrosis Factor-alpha
Recurrence
staphylococcal enterotoxin B
Incidence
T-Lymphocytes
Superantigens
Myelin Sheath
Autoimmune Diseases
Disease Progression

Keywords

  • Autoimmunity
  • Experimental allergic encephalomyelitis
  • Interleukin-10
  • Transforming growth factor-β
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Immunology

Cite this

Staphylococcal enterotoxin B and tumor-necrosis factor-α-induced relapses of experimental allergic encephalomyelitis : Protection by transforming growth factor-β and interleukin-10. / Crisi, Giovanna M.; Santambrogio, Laura; Hochwald, Gerald M.; Smith, Sidney R.; Carlino, Joseph A.; Thorbecke, G. Jeanette.

In: European Journal of Immunology, Vol. 25, No. 11, 11.1995, p. 3035-3040.

Research output: Contribution to journalArticle

Crisi, Giovanna M. ; Santambrogio, Laura ; Hochwald, Gerald M. ; Smith, Sidney R. ; Carlino, Joseph A. ; Thorbecke, G. Jeanette. / Staphylococcal enterotoxin B and tumor-necrosis factor-α-induced relapses of experimental allergic encephalomyelitis : Protection by transforming growth factor-β and interleukin-10. In: European Journal of Immunology. 1995 ; Vol. 25, No. 11. pp. 3035-3040.
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abstract = "A study was made of the ability of the superantigen staphylococcal enterotoxin B (SEB) to induce relapses of experimental allergic encephalomyelitis (EAE) in SJL mice that had partially or completely recovered from acute EAE. We find that a single injection of 0.05 mg SEB i.v. induces mild relapses in 50{\%} of such mice. In addition, tumor necrosis factor (TNF)-α (0.2 μg, i.p.) also induces EAE relapses in 43{\%} of SJL mice when injected 1-2 months after recovery. SEB does not induce a second relapse if reinjected when Vβ17a+ T cells are still partially deleted. In these mice, however, TNF-α is equally effective in inducing relapses as in mice that did not receive SEB previously. We showed earlier that transforming growth factor (TGF)-β and TNF-α have antagonistic effects on experimental autoimmune diseases; e.g., in spontaneously relapsing EAE, TGF-β and anti-TNF were protective, while anti-TGF-β caused disease exacerbation. Interleukin (IL)-10 is also known to counteract certain TNF effects. We now find that both human IL-10 and TGF-β2 lower the incidence of EAE relapses when given simultaneously with SEB or TNF-α. The protective effect of TGF-β is significant only against relapses induced by SEB (reduced to 9{\%}), and that of IL-10 only against relapses induced by TNF (reduced to 0{\%}) with the treatment regimens employed. Neutralizing anti-TGF-β does not increase the incidence of SEB-induced EAE relapses. In contrast, anti-IL-10 increases both the incidence and the severity of such relapses. We conclude that TNF production is probably important in causing EAE relapses, but that other aspects of the SEB-induced reactivation of myelin-specific T cells also contribute. Furthermore, endogenous IL-10 rather than TGF-β production appears to limit the susceptibility to induction of EAE relapses in this model.",
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