Research Papers: Immunology:
Regulatory T cells characterized by low Id3 expression are highly suppressive and accumulate during chronic infection
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Katharina S. Rauch1,2, Miriam Hils1,2, Alexandra J. Menner1,2, Mikael Sigvardsson3, Susana Minguet1,2,4, Peter Aichele1,5, Christian Schachtrup6 and Kristina Schachtrup1,2
1Center for Chronic Immunodeficiency (CCI), Medical Center – University of Freiburg, Faculty of Medicine, Freiburg, Germany
2Faculty of Biology, Freiburg, Germany
3Institution for Clinical and Experimental Sciences, Faculty of Health Sciences, Linköping University, Linköping, Sweden
4Centre for Biological Signalling Studies BIOSS, University of Freiburg, Germany and Max Planck Institute of Immunology and Epigenetics, Freiburg, Germany
5Institute for Immunology, Medical Center, University of Freiburg, Faculty of Medicine, Freiburg, Germany
6Institute of Anatomy and Cell Biology, Faculty of Medicine, Freiburg, Germany
Kristina Schachtrup, email: [email protected]
Keywords: Treg cells; chronic infection; transcription; Id proteins; immunology
Received: September 26, 2017 Accepted: October 10, 2017 Published: October 27, 2017
Foxp3+ regulatory T (Treg) cells are broadly divided into naive-like and activated Treg cells, however recent studies suggest further Treg cell heterogeneity. Treg cells contribute to impaired T cell responses in chronic infections, but the role of specific Treg cell subpopulations in viral infections is not well defined. Here, we report that activated Treg cells are separated into two transcriptionally distinct subpopulations characterized by low or high expression of the transcriptional regulator Id3. Id3lo Treg cells are a highly suppressive Treg cell subpopulation, expressing elevated levels of immunomodulatory molecules and are capable of broadly targeting T cell responses. Viral infection and interleukin-2 promote the differentiation of Id3hi into Id3lo Treg cells and during chronic infection Id3lo Treg cells are the predominant Treg cell population. Thus, our report provides a framework, in which different activated Treg cell subpopulations specifically affect immune responses, possibly contributing to T cell dysfunction in chronic infections.
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