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Adaptive Immune Response in JAM-C-Deficient Mice: Normal Initiation but Reduced IgG Memory¹

Claudia Zimmerli^*, Boris P. L. Lee^*, Gaby Palmer^*,, Cem Gabay^*,, Ralf Adams, Michel Aurrand-Lions^2,* and Beat A. Imhof^3,*

^* Department of Pathology and Immunology, University of Geneva School of Medicine, Geneva, Switzerland; Division of Rheumatology, Department of Internal Medicine, University Hospital, Geneva, Switzerland and Department of Pathology and Immunology, University of Geneva School of Medicine, Geneva, Switzerland; Max Planck Institute for Molecular Biomedecine, Department of Tissue Morphogenesis, Münster, Germany

We have recently shown that junctional adhesion molecule (JAM)-C-deficient mice have leukocytic pulmonary infiltrates, disturbed neutrophil homeostasis, and increased postnatal mortality. This phenotype was partially rescued when mice were housed in ventilated isolators, suggesting an inability to cope with opportunistic infections. In the present study, we further examined the adaptive immune responses in JAM-C^–/– mice. We found that murine conventional dendritic cells express in addition to Mac-1 and CD11c also JAM-B as ligand for JAM-C. By in vitro adhesion assay, we show that murine DCs can interact with recombinant JAM-C via Mac-1. However, this interaction does not seem to be necessary for dendritic cell migration and function in vivo, even though JAM-C is highly expressed by lymphatic sinuses of lymph nodes. Nevertheless, upon immunization and boosting with a protein Ag, JAM-C-deficient mice showed decreased persistence of specific circulating Abs although the initial response was normal. Such a phenotype has also been observed in a model of Ag-induced arthritis, showing that specific IgG2a Ab titers are reduced in the serum of JAM-C^–/– compared with wild-type mice. Taken together, these data suggest that JAM-C deficiency affects the adaptive humoral immune response against pathogens, in addition to the innate immune system.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Swiss National Science Foundation (310000-120184/1) and the Swiss Cancer League (OCS-01653-02-2005) (to B.A.I.).

² Current address: UMR891, Inserm, Centre de Recherche en Cancérologie de Marseille, Institut Paoli-Calmettes, 27, bd Leï Roure, Marseille, France.

³ Address correspondence and reprint requests to: Prof. Beat Imhof, Universite de Geneve, 1 rue Michel Servet, Geneva, Switzerland. E-mail address: Beat.Imhof{at}unige.ch

⁴ Abbreviations used in this paper: JAM, junctional adhesion molecule; DC, dendritic cell; WT, wild type; BM-DC, bone-marrow derived DC; NP-CGG, chicken -globulin; TNCB, 2,4,6-trinitrochlorobenzene; mBSA, methylated BSA; pDC, plasmacytoid DC; cDC, conventional DC; CHS, contact hypersensitivity; AIA, Ag-induced arthritis; 7-AAD, 7-aminoactinomycin D; GC, germinal center; FDC, follicular dendritic cell; LYVE, lymphatic vessel endothelial receptor; CMTMR, 5- and 6-(((4-chloromethyl)benzoyl)amino)tetramethylrhodamine.