IL-17A Promotes Pulmonary B-1a Cell Differentiation via Induction of Blimp-1 Expression during Influenza Virus Infection
Fig 3
IL-17A deficiency impairs plasmacytic differentiation of B-1a cells during influenza infection.
(A) Morphology of B-1a cells from the pleural cavity of naïve mice, or pleural cavity and lung tissues of H1N1-infected WT and Il17a-/- mice at 5 dpi was examined by cytospin preparation and Wright’s staining. (B) Mean fluorescent intensity (MFI) of CD138 expression on B-1a cells from pleural cavity of naïve mice, or pleural cavity and lung tissues of H1N1-infected WT and Il17a-/- mice were examined with flow cytometry. (n = 3). (C) B-1a cells from pleural cavity and lung tissue of H1N1-infected WT and Il17a-/- mice (n = 6) at 0 or 5 dpi were sorting purified and pooled together. Production of total IgM, virus-specific IgM and PC-specific IgM was detected with ELISPOT. Representative ELISPOT profiles of B-1a cells isolated from indicated organs of naïve or H1N1-infected mice are shown. Data are representative of two independent experiments. (D) ELISPOT analysis of total and virus-specific IgM producing B-1a cells as in (C). (E) ELISA analysis of total and virus-specific IgM in supernatants of cultured cells as in (C). (F) IgM secretion per B-1a cell was quantified based upon IgM detected in culture supernatants in (E) and correlated spot frequencies detected by ELISPOT in (D). Data are represented as mean ± SEM. n = 3. *, p < 0.05, **, p < 0.01.