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Sex-specific adipose tissue imprinting of regulatory T cells. 2020
Ajithkumar Vasanthakumar, and
David Chisanga, and
Jonas Blume, and
Renee Gloury, and
Kara Britt, and
Darren C Henstridge, and
Yifan Zhan, and
Santiago Valle Torres, and
Sebastian Liene, and
Nicholas Collins, and
Enyuan Cao, and
Tom Sidwell, and
Chaoran Li, and
Raul German Spallanzani, and
Yang Liao, and
Paul A Beavis, and
Thomas Gebhardt, and
Natalie Trevaskis, and
Stephen L Nutt, and
Jeffrey D Zajac, and
Rachel A Davey, and
Mark A Febbraio, and
Diane Mathis, and
Wei Shi, and
Axel Kallies
Department of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Victoria, Australia. ajith.vasanthakumar@unimelb.edu.au.
Adipose tissue is an energy store and a dynamic endocrine organ1,2. In particular, visceral adipose tissue (VAT) is critical for the regulation of systemic metabolism3,4. Impaired VAT function-for example, in obesity-is associated with insulin resistance and type 2 diabetes5,6. Regulatory T (Treg) cells that express the transcription factor FOXP3 are critical for limiting immune responses and suppressing tissue inflammation, including in the VAT7-9. Here we uncover pronounced sexual dimorphism in Treg cells in the VAT. Male VAT was enriched for Treg cells compared with female VAT, and Treg cells from male VAT were markedly different from their female counterparts in phenotype, transcriptional landscape and chromatin accessibility. Heightened inflammation in the male VAT facilitated the recruitment of Treg cells via the CCL2-CCR2 axis. Androgen regulated the differentiation of a unique IL-33-producing stromal cell population specific to the male VAT, which paralleled the local expansion of Treg cells. Sex hormones also regulated VAT inflammation, which shaped the transcriptional landscape of VAT-resident Treg cells in a BLIMP1 transcription factor-dependent manner. Overall, we find that sex-specific differences in Treg cells from VAT are determined by the tissue niche in a sex-hormone-dependent manner to limit adipose tissue inflammation.
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