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  4. B lymphocytes undergo TLR2-dependent apoptosis upon Shigella infection
 
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2014
Journal Article
Titel

B lymphocytes undergo TLR2-dependent apoptosis upon Shigella infection

Abstract
Antibody-mediated immunity to Shigella, the causative agent of bacillary dysentery, requires several episodes of infection to get primed and is short-lasting, suggesting that the B cell response is functionally impaired. We show that upon ex vivo infection of human colonic tissue, invasive S. flexneri interacts with and occasionally invades B lymphocytes. The induction of a type three secretion apparatus (T3SA)-dependent B cell death is observed in the human CL-01 B cell line in vitro, as well as in mouse B lymphocytes in vivo. In addition to cell death occurring in Shigella-invaded CL-01 B lymphocytes, we provide evidence that the T3SA needle tip protein IpaD can induce cell death in noninvaded cells. IpaD binds to and induces B cell apoptosis via TLR2, a signaling receptor thus far considered to result in activation of B lymphocytes. The presence of bacterial co-signals is required to sensitize B cells to apoptosis and to up-regulate tlr2, thus enhancing IpaD binding. Apoptotic B lymphocytes in contact with Shigella-IpaD are detected in rectal biopsies of infected individuals. This study therefore adds direct B lymphocyte targeting to the diversity of mechanisms used by Shigella to dampen the host immune response.
Author(s)
Nothelfer, K.
Arena, E.T.
Pinaud, L.
Neunlist, M.
Mozeleski, B.
Belotserkovsky, I.
Parsot, C.
Dinadayala, P.
Burger-Kentischer, A.
Raqib, R.
Sansonetti, P.J.
Phalipon, A.
Zeitschrift
Journal of Experimental Medicine
Thumbnail Image
DOI
10.1084/jem.20130914
Language
English
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