| Literature DB >> 25784146 |
Ping Chen1, Alastair Denniston2, Susan Hannes1, William Tucker1, Lai Wei1, Baoying Liu1, Tiaojiang Xiao3, Sima Hirani1, Zhiyu Li1, Shayma Jawad1, Han Si1, Richard W J Lee4, H Nida Sen1, Robert B Nussenblatt5.
Abstract
In this study we investigated the role of blood CD1c(+) myeloid dendritic cells 1 (mDC1), a key mDC subtype, in patients with autoimmune uveitis. We observed a significant increase of blood CD1c(+) mDC1 in uveitis patients. The increased CD1c(+) mDC1 exhibited high HLADR expression and less antigen uptake. CD1c(+) mDC1 were divided into two subpopulations. CD1c(hi) mDC1 subpopulation showed less antigen uptake and higher HLADR expression compared to CD1c(lo) mDC1 subpopulation. Importantly, the CD1c(hi) mDC1 subpopulation was increased in uveitis patients. In vitro, mature monocyte-derived dendritic cells (MoDCs), characterized by lower levels of antigen uptake, induced more CD4(+)CD62L(-) T helper cell proliferation. The mature phenotype and function of CD1c(+) mDC1 were regulated by TNFα via a p38 MAPK-dependent pathway. These data show that alterations in the systemic immune response are involved in the pathogenesis of autoimmune uveitis and invite the therapeutic possibility of attenuating uveitis by manipulating blood CD1c(+) mDC1. Published by Elsevier Inc.Entities:
Keywords: Antigen uptake; Autoimmune uveitis; CD1c(+) mDC1; CD1c(hi) mDC1 subpopulation; TNFα; p38 MAPK
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Year: 2015 PMID： 25784146 PMCID： PMC4420697 DOI： 10.1016/j.clim.2015.03.002
Source DB: PubMed Journal: Clin Immunol ISSN： 1521-6616 Impact factor: 3.969