Sphingosine-1-phosphate receptor 2 restrains egress of γδ T cells from the skin
Autor: | Jason G. Cyster, Yang Zhang, Elizabeth E. Gray, Brian J. Laidlaw, Francisco Ramírez-Valle |
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Rok vydání: | 2019 |
Předmět: |
Receptors
CCR6 T cell Immunology Population Inbred C57BL Real-Time Polymerase Chain Reaction Medical and Health Sciences 03 medical and health sciences Mice 0302 clinical medicine Antigen Dermis Cell Movement Receptors medicine Immunology and Allergy Animals education Lymph node Sphingosine-1-Phosphate Receptors S1PR1 Research Articles 030304 developmental biology S1PR2 Skin gamma-delta 0303 health sciences education.field_of_study Chemistry Brief Definitive Report Receptors Antigen T-Cell gamma-delta T-Cell Flow Cytometry Cell biology Mice Inbred C57BL medicine.anatomical_structure T cell migration CCR6 030215 immunology |
Zdroj: | The Journal of Experimental Medicine The Journal of experimental medicine, vol 216, iss 7 |
ISSN: | 1540-9538 |
Popis: | Tissue residence of motile lymphocytes depends on systems that counteract egress-promoting cues. Laidlaw et al. find that the migration inhibitory S1PR2 receptor cooperates with CD69 to promote the retention of IL-17–producing γδ T cells within the dermis. Maintenance of a population of IL-17–committed γδ T cells in the dermis is important in promoting tissue immunity. However, the signals facilitating γδ T cell retention within the dermis remain poorly understood. Here, we find that sphingosine-1-phosphate receptor 2 (S1PR2) acts in a cell-intrinsic manner to oppose γδ T cell migration from the dermis to the skin draining lymph node (dLN). Migration of dermal γδ T cells to the dLN under steady-state conditions occurs in an S1PR1-dependent manner. S1PR1 and CD69 are reciprocally expressed on dermal γδ T cells, with loss of CD69 associated with increased S1PR1 expression and enhanced migration to the dLN. γδ T cells lacking both S1PR2 and CD69 are impaired in their maintenance within the dermis. These findings provide a mechanism for how IL-17+ γδ T cells establish residence within the dermis and identify a role for S1PR2 in restraining the egress of tissue-resident lymphocytes. Graphical Abstract |
Databáze: | OpenAIRE |
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