期刊
JOURNAL OF INFECTIOUS DISEASES
卷 218, 期 8, 页码 1314-1323出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiy296
关键词
regulatory T cells; inhibitory molecules; PD-1; Plasmodium vivax; malaria
资金
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [PQ-307408/2016-7]
- Fundacao de Amparo a Pesquisa do Estado de Minas Gerais [APQ-00616-16]
- CNPq/FAPEMIG-National Institute of Science and Technology for Vaccines [CNPq-573547/2008-4/FAPEMIG/ MS-CBB-APQ00077-09]
- FAPEMIG, PRONEX-Malaria [CBB-APQ-01355-14]
- National Institute of Allergy and Infectious Diseases [NIH/NIAID/ICEMR/ U19 AI089681]
- CNPq/Ciencias sem fronteiras [402553/2012-8]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior
The balance between pro- and antiinflammatory mechanisms is essential to limit immune-mediated pathology, and CD4(+) forkhead box P3 (Foxp3(+)) regulatory T cells (Treg) play an important role in this process. The expression of inhibitory receptors regulates cytokine production by Plasmodium vivax-specific T cells. Our goal was to assess the induction of programmed death-1 (PD-1) and cytotoxic T-lymphocyte antigen (CTLA-4) on Treg during malaria and to evaluate their function. We found that P. vivax infection triggered an increase in circulating Treg and their expression of CTLA-4 and PD-1. Functional analysis demonstrated that Treg from malaria patients had impaired suppressive ability and PD-1(+)Treg displayed lower levels of Foxp3 and Helios, but had higher frequencies of T-box transcription factor(+) and interferon-gamma(+) cells than PD-1(-)Treg. Thus malaria infection alters the function of circulating Treg by triggering increased expression of PD-1 on Treg that is associated with decreased regulatory function and increased proinflammatory characteristics.
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