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

Author:

Márquez Ana Citlali,Croft Carys,Shanina Iryna,Horwitz Marc Steven

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 Th1 response, yet are important in driving infiltration of the CNS by CD8+ T cells. Given the importance of type I IFNs in MS, we used IFNARko mice in order to determine if type I IFN signaling was important in the enhancement of EAE in latently infected mice. We found that while type I IFNs are important for the control of γHV-68 infection and maintenance of latency, they do not have a direct effect in the development of enhanced EAE.

Funder

Multiple Sclerosis Society of Canada

Publisher

Frontiers Media SA

Subject

Immunology,Immunology and Allergy

Reference22 articles.

Cited by 2 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. The EBV-MS connection: the enigma remains;Frontiers in Immunology;2024-08-29

2. The innate and T-cell mediated immune response during acute and chronic gammaherpesvirus infection;Frontiers in Cellular and Infection Microbiology;2023-03-31

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