TLR3 Signaling is Required for Robust Extrafollicular B Cell Response (EF) in Influenza A/PR/8 Infection

نویسندگان

چکیده

Abstract Following influenza A virus (IAV) infection B cells rapidly proliferate and differentiate into plasma (PCs) in extrafollicular foci (EF) within mediastinal lymph nodes (medLN), resulting protective antibody secretion. We had shown that co-expression of both TLR adaptor proteins, TRIF MyD88, is required for robust EF responses. Only two TLRs, TLR3 4, signal using TRIF. As previously 7, but not TLR4, expression were upregulated by medLN 2 days post (dpi) a Type-I IFN-dependent manner, suggesting might utilize during IAV infection. To test this we generated MyD88 × double-deficient (DKO) mice. Flow cytometry on MedLN at 7 dpi showed significantly reduced (CD19 loB220 loCD38 loCD24 hi) CD138 +plasma (PCs), including IAV-specific PCs, as well serum IgG 2Cin DKO compared to C57BL/6 or single- deficient mixed bone marrow chimeras indicated the TLR3-TRIF axis contributes formation least part cell-intrinsic manner. In vitro stimulation with agonist, Poly: IC, caused several activation/costimulatory molecules did induce proliferation. Together, data suggest TLR3-mediated cell non-redundant driver rapid Supported NIH/NIAID R01AI117890 (NB) NIH T32 HL007013-40 (JHL EJK).

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ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.59.26