Direct visualization of endogenous Salmonella‐specific B cells reveals a marked delay in clonal expansion and germinal center development. Issue 2 (20th November 2014)

• Record Type: Journal Article
• Authors: Nanton, Minelva R.; Lee, Seung‐Joo; Atif, Shaikh M.; Nuccio, Sean‐Paul; Taylor, Justin J.; Bäumler, Andreas J.; Way, Sing Sing; McSorley, Stephen J.
• Is Part Of: European journal of immunology. Volume 45:Issue 2(2015:Feb.)
• Page Start: 428
• Page End: 441
• Publication Date: 2014-11-20
• Subjects: Immunology -- Periodicals; 616.079
• DOI: 10.1002/eji.201444540
• Languages: English
• ISSNs: 0014-2980

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>CD4⁺ T cells and B cells are both essential for acquired immunity to <italic>Salmonella</italic> infection. It is well established that <italic>Salmonella</italic> inhibit host CD4⁺ T‐cell responses, but a corresponding inhibitory effect on B cells is less well defined. Here, we utilize an Ag tetramer and pull‐down enrichment strategy to directly visualize OVA‐specific B cells in mice, as they respond to infection with <italic>Salmonella</italic>‐OVA. Surprisingly, OVA‐specific B‐cell expansion and germinal center formation was not detected until bacteria were cleared from the host. Furthermore, <italic>Salmonella</italic> infection also actively inhibited both B‐ and T‐cell responses to the same coinjected Ag but this did not require the presence of iNOS. The <italic>Salmonella</italic> Pathogenicity Island 2 (SPI2) locus has been shown to be responsible for inhibition of <italic>Salmonella</italic>‐specific CD4⁺ T‐cell responses, and an examination of SPI2‐deficient bacteria demonstrated a recovery in B‐cell expansion in infected mice. Together, these data suggest that <italic>Salmonella</italic> can simultaneously inhibit host B‐ and T‐cell responses using SPI2‐dependent mechanisms.</p> </abstract>