CD69 modulates sphingosine-1-phosphate-induced migration of skin dendritic cells

Lamana, Amalia; Martin, Pilar; de la Fuente, Hortensia; Martinez-Muñoz, Laura; Cruz-Adalia, Aranzazu; Ramirez-Huesca, Marta; Escribano, Cristina; Gollmer, Kathrin; Mellado, Mario; Stein, Jens V; Rodriguez-Fernandez, Jose Luis; Sanchez-Madrid, Francisco; del Hoyo, Gloria Martinez (2011). CD69 modulates sphingosine-1-phosphate-induced migration of skin dendritic cells. Journal of Investigative Dermatology, 131(7), pp. 1503-12. New York, N.Y.: Nature Publishing 10.1038/jid.2011.54

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In this study, we have investigated the role of CD69, an early inducible leukocyte activation receptor, in murine dendritic cell (DC) differentiation, maturation, and migration. Skin DCs and DC subsets present in mouse lymphoid organs express CD69 in response to maturation stimuli. Using a contact sensitization model, we show that skin DCs migrated more efficiently to draining lymph nodes (LNs) in the absence of CD69. This was confirmed by subcutaneous transfer of CD69-/- DCs, which presented an increased migration to peripheral LNs. Two-photon microscopy analysis showed that once DCs reached the LNs, CD69 deficiency did not alter DC interstitial motility in the LNs. Chemotaxis to sphingosine-1-phosphate (S1P) was enhanced in CD69-/- DCs compared with wild-type DCs. Accordingly, we detected a higher expression of S1P receptor type-1 (S1P(1)) by CD69-/- DCs, whereas S1P(3) expression levels were similar in wild-type and CD69-/- DCs. Moreover, in vivo treatment with S1P analogs SEW2871 and FTY720 during skin sensitization reduced skin DC migration to peripheral LNs. These results suggest that CD69 regulates S1P-induced skin DC migration by modulating S1P(1) function. Together, our findings increase our knowledge on DC trafficking patterns in the skin, enabling the development of new directed therapies using DCs for antigen (Ag) delivery.

Item Type:	Journal Article (Original Article)
Division/Institute:	04 Faculty of Medicine > Pre-clinic Human Medicine > Theodor Kocher Institute
UniBE Contributor:	Stein, Jens Volker
ISSN:	0022-202X
Publisher:	Nature Publishing
Language:	English
Submitter:	Factscience Import
Date Deposited:	04 Oct 2013 14:23
Last Modified:	05 Dec 2022 14:06
Publisher DOI:	10.1038/jid.2011.54
PubMed ID:	21412255
Web of Science ID:	000291644900018
URI:	https://boris.unibe.ch/id/eprint/7812 (FactScience: 213153)