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Superantigens induce primary T cell responses to soluble autoantigens by a non-V beta-specific mechanism of bystander activation.
Cell Immunol. 1995 Apr 01; 161(2):158-65.CI

Abstract

Superantigens have been suggested to act as powerful TCR V beta-specific inducers of T cell reactivity in autoimmune diseases. We have investigated the capacity of staphylococcal enterotoxins (SE) to prime autoreactive T cell responses in naive animals in the Lewis rat model of experimental autoimmune encephalomyelitis (EAE), where myelin basic protein (MBP)-specific CD4+ effector T cells express almost exclusively V beta 8.2 TCR elements. By taking advantage of the reactivity of V beta 8.2+ MBP-specific T cells to SEE but not to other SEs in vitro, we estimated the potential of different SEs (SEA, SEB, and SEE) to induce a primary T cell response to soluble MBP in vivo. Upon immunization of naive rats with soluble MBP alone or MBP and SEB (which is only a very weak superantigen for rat T cells), no MBP-responses could be retrieved. Similarly, when coimmunizing naive rats with MBP and V beta 8.2-activating SEE, no autoreactivity was inducible. By contrast, coimmunization of animals with soluble MBP and the superantigen SEA that is strongly activating various T cell subpopulations in Lewis rats but not V beta 8.2+ (i.e., potentially MBP reactive) T cells led to a significant primary MBP-specific T cell autoreactivity. These SEA-induced MBP-reactive T cells expressed V beta 8.2 TCRs at levels similar to those seen in autoreactive T cells conventionally induced by immunization with MBP administered in complete Freund's adjuvant (CFA) and could induce disease in a transfer model of EAE. Thus, our results are consistent with the notion that superantigens are able to induce primary T cell responses to soluble autoantigens by a non-V beta specific mechanism of bystander priming.

Authors+Show Affiliations

INSERM U.283, Hôpital Cochin, Université René Descartes, Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7535195

Citation

Rott, O, et al. "Superantigens Induce Primary T Cell Responses to Soluble Autoantigens By a non-V Beta-specific Mechanism of Bystander Activation." Cellular Immunology, vol. 161, no. 2, 1995, pp. 158-65.
Rott O, Mignon-Godefroy K, Fleischer B, et al. Superantigens induce primary T cell responses to soluble autoantigens by a non-V beta-specific mechanism of bystander activation. Cell Immunol. 1995;161(2):158-65.
Rott, O., Mignon-Godefroy, K., Fleischer, B., Charreire, J., & Cash, E. (1995). Superantigens induce primary T cell responses to soluble autoantigens by a non-V beta-specific mechanism of bystander activation. Cellular Immunology, 161(2), 158-65.
Rott O, et al. Superantigens Induce Primary T Cell Responses to Soluble Autoantigens By a non-V Beta-specific Mechanism of Bystander Activation. Cell Immunol. 1995 Apr 1;161(2):158-65. PubMed PMID: 7535195.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Superantigens induce primary T cell responses to soluble autoantigens by a non-V beta-specific mechanism of bystander activation. AU - Rott,O, AU - Mignon-Godefroy,K, AU - Fleischer,B, AU - Charreire,J, AU - Cash,E, PY - 1995/4/1/pubmed PY - 1995/4/1/medline PY - 1995/4/1/entrez SP - 158 EP - 65 JF - Cellular immunology JO - Cell Immunol VL - 161 IS - 2 N2 - Superantigens have been suggested to act as powerful TCR V beta-specific inducers of T cell reactivity in autoimmune diseases. We have investigated the capacity of staphylococcal enterotoxins (SE) to prime autoreactive T cell responses in naive animals in the Lewis rat model of experimental autoimmune encephalomyelitis (EAE), where myelin basic protein (MBP)-specific CD4+ effector T cells express almost exclusively V beta 8.2 TCR elements. By taking advantage of the reactivity of V beta 8.2+ MBP-specific T cells to SEE but not to other SEs in vitro, we estimated the potential of different SEs (SEA, SEB, and SEE) to induce a primary T cell response to soluble MBP in vivo. Upon immunization of naive rats with soluble MBP alone or MBP and SEB (which is only a very weak superantigen for rat T cells), no MBP-responses could be retrieved. Similarly, when coimmunizing naive rats with MBP and V beta 8.2-activating SEE, no autoreactivity was inducible. By contrast, coimmunization of animals with soluble MBP and the superantigen SEA that is strongly activating various T cell subpopulations in Lewis rats but not V beta 8.2+ (i.e., potentially MBP reactive) T cells led to a significant primary MBP-specific T cell autoreactivity. These SEA-induced MBP-reactive T cells expressed V beta 8.2 TCRs at levels similar to those seen in autoreactive T cells conventionally induced by immunization with MBP administered in complete Freund's adjuvant (CFA) and could induce disease in a transfer model of EAE. Thus, our results are consistent with the notion that superantigens are able to induce primary T cell responses to soluble autoantigens by a non-V beta specific mechanism of bystander priming. SN - 0008-8749 UR - https://www.unboundmedicine.com/medline/citation/7535195/Superantigens_induce_primary_T_cell_responses_to_soluble_autoantigens_by_a_non_V_beta_specific_mechanism_of_bystander_activation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0008-8749(85)71022-2 DB - PRIME DP - Unbound Medicine ER -