Occludin Expression in Epidermal γδ T Cells in Response to Epidermal Stress Causes Them To Migrate into Draining Lymph Nodes

• Published in: The Journal of immunology (1950) Vol. 199; no. 1; pp. 62 - 71
• Main Authors: Saito, Takahito, Yano, Michihiro, Ohki, Yutaro, Tomura, Michio, Nakano, Naoko
• Format: Journal Article
• Language: English
• Published: United States American Association of Immunologists 01.07.2017
• Subjects: Allergens; Animals; Cell activation; Cell Movement; Contact dermatitis; Dermatitis, Contact - immunology; Epidermis; Epidermis - cytology; Epidermis - immunology; Epidermis - radiation effects; Hypersensitivity; Immune response; Immunologic Surveillance; Immunosurveillance; Lymph nodes; Lymph Nodes - immunology; Lymphatic system; Lymphocyte Activation; Lymphocytes; Lymphocytes T; Mice; Mice, Inbred C57BL; Mice, Knockout; Occludin - genetics; Receptors, Antigen, T-Cell, gamma-delta - immunology; Skin; Skin - immunology; Stress; Stress, Physiological; T cell receptors; T-Lymphocyte Subsets - immunology; T-Lymphocyte Subsets - physiology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.1600848

Epidermal γδ T cells that reside in the front line of the skin play a pivotal role in stress immune surveillance. However, it is not clear whether these cells are involved in further induction of immune responses after they are activated in dysregulated epidermis. In this study, we found that activated γδ T cells expressed occludin and migrated into draining lymph nodes in an occludin-dependent manner. Epidermal γδ T cells in occludin-deficient mice exhibited impairments in morphology changes and motility, although they expressed activation markers at levels comparable to those in wild-type cells. Occludin deficiency weakened the induction of allergen-induced contact hypersensitivity, primarily as the result of the impaired migration of epidermal γδ T cells. Thus, occludin expression by epidermal γδ T cells upon activation in response to epidermal stress allows them to move, which could be important for augmentation of immune responses via collaboration with other cells.