Author
Listed:
- Nicholas Collins
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- Xiaodong Jiang
(Brigham and Women’s Hospital, Harvard Medical School)
- Ali Zaid
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- Bethany L. Macleod
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- Jane Li
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- Chang Ook Park
(Brigham and Women’s Hospital, Harvard Medical School)
- Ashraful Haque
(Malaria Immunology Laboratory, QIMR Berghofer Medical Research Institute and Australian Infectious Diseases Research Centre, The University of Queensland)
- Sammy Bedoui
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- William R. Heath
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- Scott N. Mueller
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- Thomas S. Kupper
(Brigham and Women’s Hospital, Harvard Medical School)
- Thomas Gebhardt
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
- Francis R. Carbone
(The University of Melbourne
Peter Doherty Institute for Infection and Immunity, The University of Melbourne)
Abstract
Although memory T cells within barrier tissues can persist as permanent residents, at least some exchange with blood. The extent to which this occurs is unclear. Here we show that memory CD4+ T cells in mouse skin are in equilibrium with the circulation at steady state. These cells are dispersed throughout the inter-follicular regions of the dermis and form clusters with antigen presenting cells around hair follicles. After infection or administration of a contact sensitizing agent, there is a sustained increase in skin CD4+ T-cell content, which is confined to the clusters, with a concomitant CCL5-dependent increase in CD4+ T-cell recruitment. Skin CCL5 is derived from CD11b+ cells and CD8+ T cells, with the elimination of the latter decreasing CD4+ T-cell numbers. These results reveal a complex pattern of tissue-retention and equilibration for CD4+ memory T cells in skin, which is altered by infection and inflammation history.
Suggested Citation
Nicholas Collins & Xiaodong Jiang & Ali Zaid & Bethany L. Macleod & Jane Li & Chang Ook Park & Ashraful Haque & Sammy Bedoui & William R. Heath & Scott N. Mueller & Thomas S. Kupper & Thomas Gebhardt , 2016.
"Skin CD4+ memory T cells exhibit combined cluster-mediated retention and equilibration with the circulation,"
Nature Communications, Nature, vol. 7(1), pages 1-13, September.
Handle:
RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11514
DOI: 10.1038/ncomms11514
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