γδ T cells compose a developmentally regulated intrauterine population and protect against vaginal candidiasis

Leticia Monin(The Francis Crick Institute), Dmitry S. Ushakov(King's College London), Henriette Arnesen(Norwegian University of Life Sciences), Nourdine Bah(The Francis Crick Institute), Anett Jandke(The Francis Crick Institute), Miguel Muñoz‐Ruiz(The Francis Crick Institute), Joana Carvalho(The Francis Crick Institute), Susan Joseph(Guy's Hospital), Bruna Almeida(The Francis Crick Institute), Mary Green(The Francis Crick Institute), Emma Nye(The Francis Crick Institute), Shinya Hatano(Kyushu University), Yasunobu Yoshikai(Kyushu University), Michael A. Curtis(Guy's Hospital), Harald Carlsen(Norwegian University of Life Sciences), Ulrich Steinhoff(Philipps University of Marburg), Preben Boysen(Norwegian University of Life Sciences), Adrian Hayday(King's College London)
Mucosal Immunology
May 29, 2020
Cited by 62Open Access
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Abstract

This most comprehensive analysis to date of T cells in the murine uterus reveals them to compose a unique local T-cell compartment. Consistent with earlier reports, most cells expressed a canonical V6V1 TCR, and produced interleukin (IL)-17A upon stimulation. Nonetheless, contrasting with earlier reports, uterine T cells were not obviously intraepithelial, being more akin to sub-epithelial V6V1 + T cells at several other anatomical sites. By contrast to other tissues however, the uterine compartment also included non-V6 + , IFN--producing cells; was strikingly enriched in young mice; expressed genes hitherto associated with the uterus, including the progesterone receptor; and did not require microbes for development and/or maintenance. This notwithstanding, T-cell deficiency severely impaired resistance to reproductive tract infection by Candida albicans, associated with decreased responses of IL-17-dependent neutrophils. These findings emphasise tissue-specific complexities of different mucosal cell compartments, and their evident importance in lymphoid stress-surveillance against barrier infection.


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