Interleukin-22 Drives Endogenous Thymic Regeneration in Mice

Author:

Dudakov Jarrod A.12,Hanash Alan M.3,Jenq Robert R.34,Young Lauren F.1,Ghosh Arnab1,Singer Natalie V.1,West Mallory L.1,Smith Odette M.1,Holland Amanda M.15,Tsai Jennifer J.15,Boyd Richard L.2,van den Brink Marcel R. M.1345

Affiliation:

1. Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

2. Monash Immunology and Stem Cell Laboratories, Monash University, Melbourne, Victoria 3800, Australia.

3. Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

4. Department of Medicine, Weill Cornell Medical College, New York, NY 10021, USA.

5. Department of Immunology and Microbial Pathogenesis, Weill Cornell Medical College, New York, NY 10021, USA.

Abstract

IL-22 Protects the Thymus One of the side effects associated with radiation treatment and some types of chemotherapy is damage to the thymus. Immunological T cells develop in the thymus, and so damage to this organ results in immunodeficiency and increased susceptibility to infectious disease. Although the organ eventually recovers, therapies that speed this recovery process are of interest. Dudakov et al. (p. 91 , published online 1 March; see the Perspective by Bhandoola and Artis ) now show in mice that interleukin-22 (IL-22) production in the thymus is increased in response to radiation damage and that this cytokine promotes thymic repair. After radiation treatment, IL-23 production by thymic dendritic cells induced IL-22 secretion by a population of radio-resistant innate lymphoid cells. IL-22 appeared to mediate its effects by promoting the survival and proliferation of thymic epithelial cells.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference30 articles.

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