| Literature DB >> 27448585 |
Nicholas M Provine1, Rafael A Larocca1, Malika Aid1, Pablo Penaloza-MacMaster1, Alexander Badamchi-Zadeh1, Erica N Borducchi1, Kathleen B Yates2, Peter Abbink1, Marinela Kirilova1, David Ng'ang'a1, Jonathan Bramson3, W Nicholas Haining4, Dan H Barouch5.
Abstract
CD4(+) T cell help is critical for optimal CD8(+) T cell memory differentiation and maintenance in many experimental systems. In addition, many reports have identified reduced primary CD8(+) T cell responses in the absence of CD4(+) T cell help, which often coincides with reduced Ag or pathogen clearance. In this study, we demonstrate that absence of CD4(+) T cells at the time of adenovirus vector immunization of mice led to immediate impairments in early CD8(+) T cell functionality and differentiation. Unhelped CD8(+) T cells exhibited a reduced effector phenotype, decreased ex vivo cytotoxicity, and decreased capacity to produce cytokines. This dysfunctional state was imprinted within 3 d of immunization. Unhelped CD8(+) T cells expressed elevated levels of inhibitory receptors and exhibited transcriptomic exhaustion and anergy profiles by gene set enrichment analysis. Dysfunctional, impaired effector differentiation also occurred following immunization of CD4(+) T cell-deficient mice with a poxvirus vector. This study demonstrates that following priming with viral vectors, CD4(+) T cell help is required to promote both the expansion and acquisition of effector functions by CD8(+) T cells, which is accomplished by preventing immediate dysfunction.Entities:
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Year: 2016 PMID: 27448585 PMCID: PMC4991249 DOI: 10.4049/jimmunol.1600591
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422