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Immunomodulation of experimental autoimmune encephalomyelitis by staphylococcal enterotoxin D.
Cell Immunol. 1993 Jul; 149(2):268-78.CI

Abstract

Staphylococcal enterotoxins (SEs) can bind major histocompatibility antigens and stimulate T cells which bear particular types of T cell receptor. Therefore, it has been postulated that SEs may trigger or modulate the development of autoimmune diseases caused by T cells. In the present study, we examined the effects of SEs on rat encephalitogenic T cells and the clinical manifestation of experimental autoimmune encephalomyelitis (EAE). SED, but not other SEs, stimulated encephalitogenic T cells. Furthermore, culture of lymphoid cells from myelin basic protein (MBP)-immunized rats with SED augmented the clinical manifestation of passively transferred EAE, whereas SEA and SEB showed no significant EAE-transfer ability. Flow cytometric analysis demonstrated that in vitro SED stimulation of T cells from MBP-immunized rats, but not from normal rats, resulted in selective expansion of V beta 8.2+ T cells. Consistent with in vitro findings, in vivo administration of SED modulated EAE elicited by immunization with MBP. SED given after the immunization augmented clinical manifestation, especially at low doses. On the other hand, SED given 7 days before the immunization suppressed the development of EAE in a dose-dependent manner. Interestingly, the same toxin given at a dose of 20 micrograms to thymectomized rats induced enhanced EAE regardless of the timing of administration. It has already been established that SEs stimulate T cells bearing a particular type of TCR V beta chain and subsequently induce unresponsiveness of these T cells. The present results suggest that a similar mechanism may operate in rats after the toxin treatment and MBP immunization. However, in vitro assay showed that the proliferative responses of T cells from EAE-suppressed rats to MBP and SED were not eliminated, suggesting that SED-induced suppressor T cells may also play some roles in EAE suppression. The present study has shown that SED, one of the superantigens, modulates an autoimmune disease. More importantly, its effects are not uniform, but instead are closely related to the dose of the toxin, timing of toxin exposure, and the status of hosts.

Authors+Show Affiliations

Department of Immunology, Niigata University School of Medicine, Japan.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

7687198

Citation

Matsumoto, Y, and M Fujiwara. "Immunomodulation of Experimental Autoimmune Encephalomyelitis By Staphylococcal Enterotoxin D." Cellular Immunology, vol. 149, no. 2, 1993, pp. 268-78.
Matsumoto Y, Fujiwara M. Immunomodulation of experimental autoimmune encephalomyelitis by staphylococcal enterotoxin D. Cell Immunol. 1993;149(2):268-78.
Matsumoto, Y., & Fujiwara, M. (1993). Immunomodulation of experimental autoimmune encephalomyelitis by staphylococcal enterotoxin D. Cellular Immunology, 149(2), 268-78.
Matsumoto Y, Fujiwara M. Immunomodulation of Experimental Autoimmune Encephalomyelitis By Staphylococcal Enterotoxin D. Cell Immunol. 1993;149(2):268-78. PubMed PMID: 7687198.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immunomodulation of experimental autoimmune encephalomyelitis by staphylococcal enterotoxin D. AU - Matsumoto,Y, AU - Fujiwara,M, PY - 1993/7/1/pubmed PY - 1993/7/1/medline PY - 1993/7/1/entrez SP - 268 EP - 78 JF - Cellular immunology JO - Cell Immunol VL - 149 IS - 2 N2 - Staphylococcal enterotoxins (SEs) can bind major histocompatibility antigens and stimulate T cells which bear particular types of T cell receptor. Therefore, it has been postulated that SEs may trigger or modulate the development of autoimmune diseases caused by T cells. In the present study, we examined the effects of SEs on rat encephalitogenic T cells and the clinical manifestation of experimental autoimmune encephalomyelitis (EAE). SED, but not other SEs, stimulated encephalitogenic T cells. Furthermore, culture of lymphoid cells from myelin basic protein (MBP)-immunized rats with SED augmented the clinical manifestation of passively transferred EAE, whereas SEA and SEB showed no significant EAE-transfer ability. Flow cytometric analysis demonstrated that in vitro SED stimulation of T cells from MBP-immunized rats, but not from normal rats, resulted in selective expansion of V beta 8.2+ T cells. Consistent with in vitro findings, in vivo administration of SED modulated EAE elicited by immunization with MBP. SED given after the immunization augmented clinical manifestation, especially at low doses. On the other hand, SED given 7 days before the immunization suppressed the development of EAE in a dose-dependent manner. Interestingly, the same toxin given at a dose of 20 micrograms to thymectomized rats induced enhanced EAE regardless of the timing of administration. It has already been established that SEs stimulate T cells bearing a particular type of TCR V beta chain and subsequently induce unresponsiveness of these T cells. The present results suggest that a similar mechanism may operate in rats after the toxin treatment and MBP immunization. However, in vitro assay showed that the proliferative responses of T cells from EAE-suppressed rats to MBP and SED were not eliminated, suggesting that SED-induced suppressor T cells may also play some roles in EAE suppression. The present study has shown that SED, one of the superantigens, modulates an autoimmune disease. More importantly, its effects are not uniform, but instead are closely related to the dose of the toxin, timing of toxin exposure, and the status of hosts. SN - 0008-8749 UR - https://www.unboundmedicine.com/medline/citation/7687198/Immunomodulation_of_experimental_autoimmune_encephalomyelitis_by_staphylococcal_enterotoxin_D_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0008-8749(83)71154-8 DB - PRIME DP - Unbound Medicine ER -