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B cell‐Dendritic Cell interaction during influenza infection
Author(s) -
Chen ChingI,
Lerche Jacquelyn,
Baumgarth Nicole
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.857.11
Subject(s) - biology , b cell , immunology , antigen , antigen presenting cell , immune system , respiratory tract , antibody , virus , secretion , antigen presentation , t cell , immunoglobulin class switching , lymph node , virology , cell , isotype , dendritic cell , respiratory system , monoclonal antibody , biochemistry , genetics , anatomy
Strong antibody responses against influenza virus are mounted rapidly in the respiratory tract following an infection. These B cell responses contribute to immune protection, but how they are regulated is still incompletely understood. Antigen‐presenting cells (APC) can directly support B cell activation and class switch recombination in the absence of T cells. We aimed to determine whether influenza infection‐induced respiratory tract APC support virus‐specific B cell responses. We conducted co‐culture experiments of enriched influenza virus‐specific B cells with FACS‐purified dendritic cells (DC) and macrophages from three‐day infected lung and draining lymph nodes. B cells from MCMV‐infected mice served as controls. B cell proliferation was assessed by CFSE‐staining, total and virus‐specific antibody‐secretion was measured by ELISA and the Ig isotype profile was determined by bead array. Overall, respiratory tract APC did not support clonal B cell expansion but had significant effects on virus‐specific IgG‐secretion. Surprisingly, lung APC, particularly DC, were superior in their ability to provide help compared to lymph node APC. The effects were virus‐specific and required no additional antigen. Our data provide evidence that respiratory tract APC can drive specific B cell differentiation and they suggest an important role for tissue‐resident APC in B cell response induction. NIH A1055881.