Influence of Type I Interferons in Gammaherpesvirus-68 and Its Influence on EAE Enhancement.

ABSTRACT: Epstein-Barr virus (EBV) has been identified as a putative trigger of multiple sclerosis (MS). Previously, we reported that mice latently infected with murine gammaherpesvirus 68 (γHV-68), the murine homolog to EBV, and induced for experimental autoimmune encephalomyelitis (EAE), developed an enhanced disease more reminiscent of MS. These prior results showed that expression of CD40 on CD11b⁺CD11c⁺ cells in latently infected mice was required to prime the strong Th1 response driving disease as well as decreasing Treg frequencies in the periphery and CNS. Subsequent work demonstrated that transfer of B cells from latently infected mice was sufficient to enhance disease. Herein, we show that B cells from infected mice do not need type I IFN signaling to drive a strong T

SUBMITTER: Marquez AC 

PROVIDER: S-EPMC9301468 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature