Stress down-regulates experimental allergic encephalomyelitis (EAE) but permits activation and localization of autoreactive V beta 8.2+ T cells.

Experimental allergic encephalomyelitis (EAE) is an autoimmune disease inducible by encephalitogenic helper T cells expressing V beta 8.2. In this study, we examined the relationship between the stressor-induced alternation of clinical EAE and the induction of autoreactive T cells using Lewis rats. Animals were immersed for 5 min in a water bath maintained at 44 degrees C continuously for 10 or 13 days, before or after the immunization of the encephalitogenic peptide, respectively. Stress administrations after the immunization clearly diminished the severity of clinical EAE, and delayed the onset of disease. On the other hand, stress administrations prior to the immunization resulted in the marginal suppression of clinical EAE. Splenocytes of the stressed rats showed, however, comparative proliferative responses to the encephalitogenic peptide or mitogens with that of the control rats. Moreover, higher level of V beta 8.2 mRNA expression was detected in the spinal cords of the stressed rats than in control rats. Sequence analysis of CDR3 region of TCR cDNA showed that V beta 8.2+ T cells in the spinal cords of the stressed rats possess common features with the biased encephalitogenic T cells. These results suggest that the stressor-induced suppression of clinical EAE is not simply because of the failure of induction of autoreactive T cells, nor localization of the autoreactive T cells in the central nervous system.