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© Artur Scherf
Scanning Electron Microscopy of Red Blood Cell infected by Plasmodium falciparum.
Publication : Proceedings of the National Academy of Sciences of the United States of America

γδ-T cells promote IFN-γ-dependent pathogenesis upon liver-stage infection

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Proceedings of the National Academy of Sciences of the United States of America - 26 Apr 2019

Ribot JC, Neres R, Zuzarte-Luís V, Gomes AQ, Mancio-Silva L, Mensurado S, Pinto-Neves D, Santos MM, Carvalho T, Landry JJM, Rolo EA, Malik A, Silva DV, Mota MM, Silva-Santos B, Pamplona A

Link to Pubmed [PMID] – 31028144

Proc. Natl. Acad. Sci. U.S.A. 2019 May;116(20):9979-9988

Cerebral malaria (CM) is a major cause of death due to infection. Both parasite and host factors contribute to the onset of CM, but the precise cellular and molecular mechanisms that contribute to its pathogenesis remain poorly characterized. Unlike conventional αβ-T cells, previous studies on murine γδ-T cells failed to identify a nonredundant role for this T cell subset in experimental cerebral malaria (ECM). Here we show that mice lacking γδ-T cells are resistant to ECM when infected with ANKA sporozoites, the liver-infective form of the parasite and the natural route of infection, in contrast with their susceptible phenotype if challenged with ANKA-infected red blood cells that bypass the liver stage of infection. Strikingly, the presence of γδ-T cells enhanced the expression of immunogenic factors and exacerbated subsequent systemic and brain-infiltrating inflammatory αβ-T cell responses. These phenomena were dependent on the proinflammatory cytokine IFN-γ, which was required during liver stage for modulation of the parasite transcriptome, as well as for downstream immune-mediated pathology. Our work reveals an unanticipated critical role of γδ-T cells in the development of ECM upon liver-stage infection.

https://www.ncbi.nlm.nih.gov/pubmed/31028144