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RIP2 Contributes to Expanded CD4 + T Cell IFN-γ Production during Efferocytosis of Streptococcus pneumoniae -Infected Apoptotic Cells.

Victoria Eugenia Niño CastañoLetícia de Aquino PenteadoLudmilla Silva-PereiraJúlia Miranda Ribeiro BazzanoAllan Botinhon OrlandoAna Carolina Guerta SalinaNaiara Naiana DejaniVânia L D BonatoC Henrique SerezaniAlexandra Ivo Medeiros
Published in: ImmunoHorizons (2022)
Apoptotic cell clearance by professional and nonprofessional phagocytes in the process of efferocytosis is critical to preserve tissue homeostasis. Uptake of apoptotic cells by dendritic cells generates regulatory T cells and induces immunologic tolerance against self-antigens. In contrast, ingestion of infected apoptotic cells promotes activation of TLR4/MyD88-dependent bone marrow-derived dendritic cells (BMDCs) and triggers Th17 cell differentiation. In this study, we evaluated the impact of Streptococcus pneumoniae -infected apoptotic cell efferocytosis by BMDCs derived from C57BL/6 mice on differentiation and expansion of CD4 + T cell subsets, as well as the role of TLR2/4 and receptor-interacting protein 2 (RIP2) receptors in recognizing intracellular pathogens during efferocytosis. We demonstrated that BMDC-mediated efferocytosis of S. pneumoniae -infected apoptotic cells induced Th1 cell differentiation and expansion. Although TLR2/4 and RIP2 deficiency in BMDCs did not affect Th1 cell differentiation during efferocytosis, the absence of RIP2 decreased IFN-γ production by CD4 T cells during the expansion phase. These findings suggest that RIP2-mediated IL-1β production during efferocytosis of S. pneumoniae -infected apoptotic cells partially supports a Th1-mediated IFN-γ production microenvironment.
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