TY - JOUR
T1 - Effects of staphylococcal enterotoxin B on T cell receptor Vβ utilization and clinical manifestations of experimental allergic encephalomyelitis
AU - Kalman, Bernadette
AU - Lublin, Fred D.
AU - Lattime, Edmund
AU - Joseph, Jeymohan
AU - Knobler, Robert L.
N1 - Funding Information: This work was supported by grants PP 0250 and RG 1722 from the National Multiple Sclerosis Society and NS 22145 from the National Institutes of Health of the USA.
PY - 1993/6
Y1 - 1993/6
N2 - Staphylococcal enterotoxin B (SEB) is a superantigen (SA) that up-regulates and then subsequently down-regulates and deletes T cells expressing Vβ8 T cell receptor (TcR) chains (Marrack and Kappler, 1990; Johnson et al., 1991). We have investigated the effect of SEB on experimental allergic encephalomyelitis (EAE) in PL/J mice, where the predominant encephalitogenic T cells are Vβ8+ (Acha Orbea et al., 1988; Zamvil et al., 1988). SEB did not enhance induction of EAE when administered prior to or after immunization for EAE. PL/J mice pretreated with SEB developed anergy and deletion of Vβ8 bearing cells and concomitant reduction in the incidence of EAE. Following SEB pretreatment, a redistribution in the TcR utilization of MBP-specific lymphocytes occurred. As a result, there was a low frequency of Vβ8 and expansion of other, normally less frequent, myelin basic protein (MBP)-specific clones. These observations indicate that systemic exposure to superantigen can influence organ-specific autoimmune diseases. We observed Vβ-specific elimination, rather than activation, of autoimmune clones, a finding of potential therapeutic value. Modification of the TcR repertoire by systemic exposure to this SA indicates plasticity of immune reactivity and demonstrates a mechanism by which an environmental exposure (SEB) can influence a genetically determined, T cell mediated autoimmune disease.
AB - Staphylococcal enterotoxin B (SEB) is a superantigen (SA) that up-regulates and then subsequently down-regulates and deletes T cells expressing Vβ8 T cell receptor (TcR) chains (Marrack and Kappler, 1990; Johnson et al., 1991). We have investigated the effect of SEB on experimental allergic encephalomyelitis (EAE) in PL/J mice, where the predominant encephalitogenic T cells are Vβ8+ (Acha Orbea et al., 1988; Zamvil et al., 1988). SEB did not enhance induction of EAE when administered prior to or after immunization for EAE. PL/J mice pretreated with SEB developed anergy and deletion of Vβ8 bearing cells and concomitant reduction in the incidence of EAE. Following SEB pretreatment, a redistribution in the TcR utilization of MBP-specific lymphocytes occurred. As a result, there was a low frequency of Vβ8 and expansion of other, normally less frequent, myelin basic protein (MBP)-specific clones. These observations indicate that systemic exposure to superantigen can influence organ-specific autoimmune diseases. We observed Vβ-specific elimination, rather than activation, of autoimmune clones, a finding of potential therapeutic value. Modification of the TcR repertoire by systemic exposure to this SA indicates plasticity of immune reactivity and demonstrates a mechanism by which an environmental exposure (SEB) can influence a genetically determined, T cell mediated autoimmune disease.
KW - Experimental allergic encephalomyelitis
KW - Superantigens
KW - T cell receptor
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U2 - https://doi.org/10.1016/0165-5728(93)90167-W
DO - https://doi.org/10.1016/0165-5728(93)90167-W
M3 - Article
C2 - 7687252
SN - 0165-5728
VL - 45
SP - 83
EP - 88
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -