Junctional adhesion molecules (JAM)-B and -C contribute to leukocyte extravasation to the skin and mediate cutaneous inflammation

Ralf J. Ludwig*, Thomas M. Zollner, Sentot Santoso, Katja Hardt, Jens Gille, Holger Baatz, Petra Schulze Johann, Jeannette Pfeffer, Heinfried H. Radeke, Michael P. Schön, Roland Kaufmann, Wolf Henning Boehncke, Maurizio Podda

*Corresponding author for this work
71 Citations (Scopus)


Leukocyte extravasation is a finely tuned process, in which transmigration is the final step. Transmigration depends on molecules located at borders of endothelial cells; e.g., junctional adhesion molecules (JAM-A, -B and -C). In vivo blockade of JAM-A lead to decreased migration of monocytes into the skin. In contrast, the role of JAM-B and -C in development of cutaneous inflammation is unknown. We therefore elicited an allergic contact dermatitis in mice using 2,4-dinitro-1-fluorobenzene. RT-PCR and immunofluorescent staining of healthy skin revealed a constitutive JAM-B (66.4% ± 6.7% of all vessels) and -C expression (88.6 ± 13.2%), which remained constant after induction of contact dermatitis. Functional studies, in which either JAM-B or -C neutralizing antibodies were injected into sensitized mice prior to allergen challenge showed a concentration-dependent reduction of the contact dermatitis. Decreased ear swelling was accompanied by reduction of leukocyte infiltration as analyzed by hematoxylin and eosin (H&E) histology and enzyme activity. Combined antibody treatment at doses of 1.25 mg per kg bodyweight lead to additive inhibition of allergic contact dermatitis, indicating that JAM-B and -C may have distinct functions. In conclusion, interactions with JAM-B and -C are essential for development of cutaneous inflammation.

Original languageEnglish
JournalJournal of Investigative Dermatology
Issue number5
Pages (from-to)969-976
Number of pages8
Publication statusPublished - 24.06.2005


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