Format

Send to

Choose Destination
Brain Behav Immun. 2018 Oct 1. pii: S0889-1591(18)30649-4. doi: 10.1016/j.bbi.2018.09.028. [Epub ahead of print]

Enriched environment regulates thymocyte development and alleviates experimental autoimmune encephalomyelitis in mice.

Author information

1
Department of Cancer Biology and Genetics, College of Medicine, The Ohio State University, Columbus, OH 43210, United States; The Ohio State University Comprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, Columbus, OH 43210, United States.
2
Division of Hematology, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, OH 43210, United States; The Ohio State University Comprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, Columbus, OH 43210, United States.
3
Division of Hematology, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, OH 43210, United States; The Ohio State University Comprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, Columbus, OH 43210, United States. Electronic address: mcaligiuri@coh.org.
4
Department of Cancer Biology and Genetics, College of Medicine, The Ohio State University, Columbus, OH 43210, United States; The Ohio State University Comprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, Columbus, OH 43210, United States. Electronic address: lei.cao@osumc.edu.

Abstract

Environmental and social factors have profound impacts on immune homeostasis. Our work on environmental enrichment (EE) has revealed a novel anti-obesity and anticancer phenotype associated with enhanced activity of CD8+ cytotoxic T lymphocytes in secondary lymphoid tissues. Here we investigated how an EE modulated thymus and thymocyte development. EE decreased thymus mass and cellularity, decreased the double positive thymocyte population, increased the proportion of CD8+ T cells, reduced the CD4:CD8 ratio, and downregulated CD69 expression in T cells. In a model of multiple sclerosis: experimental autoimmune encephalomyelitis (EAE), EE alleviated symptoms, inhibited spinal cord inflammation through regulation of type 1 T-helper cells mediated by glucocorticoid receptor signaling, and prevented EAE-induced thymic disturbance. Our mechanistic studies demonstrated that hypothalamic BDNF activated a hypothalamic-pituitary-adrenal axis mediating the EE's thymic effects. Our results indicate that a lifestyle intervention links the nervous, endocrine, and adaptive immune system, allowing the body to adapt to internal and external environments.

KEYWORDS:

BDNF; Environmental enrichment; Experimental autoimmune encephalomyelitis; T cell; Thymus

PMID:
30287389
DOI:
10.1016/j.bbi.2018.09.028

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center