Type 1 Treg cells promote the generation of CD8+ tissue-resident memory T cells
Authors: Marta Baptista
André Barros
Birte Blankenhaus
Hans C Probst
Cristina Ferreira
Leandro Barros
Adelheid Cerwenka
Alexandra Lainé
Patrícia Figueiredo-Campos
Špela Konjar
Ana Stojanovic
Marc Veldhoen
Julien C Marie
Nadine Kamenjarin
Journal: Nature immunology (2020)
Discipline: IMMUNOLOGY
Keywords: Tissue-resident memory T cells; TRM cells; type 1 regulatory T cells; Treg cells; T-bet
Affiliations: Instituto de Medicina Molecular, João Lobo Antunes, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal. ., Instituto de Medicina Molecular, João Lobo Antunes, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal., Innate Immunity and Inflammation, Instituto Gulbenkian de Ciência, Oeiras, Portugal., Tumor Escape Resistance Immunity Department, Cancer Research Center of Lyon, UMR INSERM1052, Lyon, France., Université Lyon 1, Lyon, France., Centre Léon Bérard, Lyon, France., Labex DEVweCAN F-69008, Lyon, France., Equipe Labelisée Ligue Nationale Contre le Cancer, Lyon, France., Institute for Immunology, University Medical Center Mainz, Mainz, Germany., Research Centre for Immunotherapy, University Medical Center Mainz, Mainz, Germany., Department of Immunobiochemistry, Mannheim Institute for Innate Immunoscience (MI3) and European Center of Angioscience (ECAS), Heidelberg University, Medical Faculty Mannheim, Mannheim, Germany.

Abstract:  Tissue-resident memory T (TRM) cells, functionally distinct from circulating memory T cells, have a critical role in protective immunity in tissues, are more efficacious when elicited after vaccination and yield more effective antitumor immunity, yet the signals that direct development of TRM cells are incompletely understood. Here we show that type 1 regulatory T (Treg) cells, which express the transcription factor T-bet, promote the generation of CD8+ TRM cells. The absence of T-bet-expressing type 1 Treg cells reduces the presence of TRM cells in multiple tissues and increases pathogen burden upon infectious challenge. Using infection models, we show that type 1 Treg cells are specifically recruited to local inflammatory sites via the chemokine receptor CXCR3. Close proximity with effector CD8+ T cells and Treg cell expression of integrin-β8 endows the bioavailability of transforming growth factor-β in the microenvironment, thereby promoting the generation of CD8+ TRM cells. 

Retracted: No

PubPeer comments:
 The title  Foxp3-dependent Tbx21 excision results in alterations in CD8+ T cell populations for figure 2 is misleading. In figure 2 F and G, the authors report that the ratio of CD4 CD8 in the intestinal lamina proproa is reduced in the Foxp3u2206Tbx21 mice while increased in the Foxp3u2206Eomes mice. However, the supplementary figure 2 A to C show that there is no difference in CD8+ T cells, expect for doudenum in Foxp3u2206Eomes mice. These data suggest that neither Foxp3u2206Tbx21 nor Foxp3u2206Eomes mice have any significant impact on the number CD8+ T cells in the intestinal lamina propria and the reported effect in figure 2F and G is due to changes in CD4+ T cells, not CD8+ T cells. ![file] , 
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