Author:
Santiago-Carvalho Igor,Almeida-Santos Gislane,Macedo Bruna Gois,Barbosa-Bomfim Caio Cesar,Almeida Fabricio Moreira,Cione Marcos Vinícios Pinheiro,Vardam-Kaur Trupti,Masuda Mia,Van Dijk Sarah,Melo Bruno Marcel,do Nascimento Rogério Silva,Souza Rebeka da Conceição,Peixoto-Rangel Alba Lucínia,Coutinho-Silva Robson,Hirata Mario H.,Alves-Filho José Carlos,Álvarez José Maria,Lassounskaia Elena,da Silva Henrique Borges,D’Império-Lima Maria Regina
Abstract
ABSTRACTCD4+ T cells are key components of the immune response during lung infections and can mediate protection against tuberculosis (TB) or influenza. However, CD4+ T cells can also promote lung pathology during these infections, making it unclear how these cells control such discrepant effects. Using mouse models of hypervirulent TB and influenza, we observed that exaggerated accumulation of parenchymal CD4+ T cells promotes lung damage. Low numbers of lung CD4+ T cells, in contrast, are sufficient to protect against hypervirulent TB. In both situations, lung CD4+ T cell accumulation is mediated by CD4+ T cell-specific expression of the extracellular ATP (eATP) receptor P2RX7. P2RX7 upregulation in lung CD4+ T cells promotes expression of the chemokine receptor CXCR3 and favors in situ proliferation. Our findings suggest that direct sensing of lung eATP by CD4+ T cells is critical to induce tissue CD4+ T cell accumulation and pathology during lung infections.GRAPHICAL ABSTRACT
Publisher
Cold Spring Harbor Laboratory
Cited by
2 articles.
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