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Roles for T and NK Cells in the Innate Immune Response to Shigella flexneri¹

Karine Le-Barillec^*, Joao Gamelas Magalhaes, Erwan Corcuff^*, Audrey Thuizat, Philippe J. Sansonetti, Armelle Phalipon^2, and James P. Di Santo^*

^* Unité des Cytokines et Développement Lymphoide, Institut National de la Santé et de la Recherche Médicale, Unité 668, and Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale, Unité 389, Institut Pasteur, Paris, France

Shigella flexneri, an enteroinvasive Gram-negative bacterium, is responsible for the worldwide endemic form of bacillary dysentery. The host response to primary infection is characterized by the induction of an acute inflammation, which is accompanied by polymorphonuclear cell (PMN) infiltration, resulting in massive destruction of the colonic mucosa. However, PMN play a major role in the recovery from primary infection, by restricting the bacterial infection at the intestinal mucosa. In this study, we assessed the roles for T and NK cells in the control of primary S. flexneri infection, using an alymphoid mouse strain (Rag°_c°) devoid of B, T, and NK cells. Using the mouse pulmonary model of Shigella infection, we showed that alymphoid Rag°_c° mice were highly susceptible to S. flexneri infection in comparison with wild-type (wt) mice. Whereas PMN recruitment upon infection was similar, macrophage recruitment and production of proinflammatory cytokines were significantly decreased in Rag°_c° mice compared with wt mice. Upon selective engraftment of Rag°_c° mice with polyclonal T cells, but not with T cells from IFN-°, S. flexneri infection could be subsequently controlled. Rag° mice devoid of B and T cells but harboring NK cells could control infection. Local IFN- production by T and NK cells recruited to the lung was demonstrated in S. flexneri-infected wt mice. These data demonstrate that both T cells and NK cells contribute to the early control of S. flexneri infection through amplification of an inflammatory response. This cellular lymphocyte redundancy assures IFN- production, which is central to innate immunity against Shigella infection.

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