In:
The Journal of Immunology, The American Association of Immunologists, Vol. 196, No. 1_Supplement ( 2016-05-01), p. 118.15-118.15
Abstract:
Multiple sclerosis (MS) starts with increased migration of auto-reactive lymphocytes across the blood-brain barrier, resulting in persistent neurodegeneration. Evidence from clinical and epidemiological studies indicated that viral infections are important in the induction of autoimmunity including MS. Using the experimental autoimmune encephalomyelitis (EAE) as a model for MS, we demonstrated that influenza infection can modulate the development of the central nervous system (CNS) inflammation. It was shown that mice with influenza infection were unable to recover from EAE, exhibiting a long-term chronic disease course. We found that the exacerbated disease after influenza virus infection was due to elevated Th1 cells infiltration into CNS, and this enhancement in the early stage of EAE disease is accompanied by increased CCR5+CD4+, CXCR3+CD4+ T cell and MOG35–55 specific CD4+ T cells localized in the lung and its draining lymph node in influenza virus-infected mice. We also observed much more CD45highCD4+CD44high effector T cell and CCR5, CXCR3, IFNγ expressing Th1 type cells entering the CNS at both acute phase and later stage of EAE disease in influenza virus-infected mice. Finally, the administration of a CCR5 and CXCR3 antagonist inhitibs the Th1 cells infiltration and significantly decreases the difference of clinical disease course between mock and influenza virus-infected mice. Taken together, our data suggested that prior influenza infection may affect subsequent EAE pathogenesis by selectively recruit CCR5 and CXCR3 bearing CD4 T cells into CNS.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.196.Supp.118.15
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2016
detail.hit.zdb_id:
1475085-5
