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

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 c...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2009-04, Vol.182 (8), p.4728-4736
Main Authors: Zimmerli, Claudia, Lee, Boris P. L, Palmer, Gaby, Gabay, Cem, Adams, Ralf, Aurrand-Lions, Michel, Imhof, Beat A
Format: Article
Language:English
Subjects:
Animals
Cell Adhesion Molecules - deficiency
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - immunology
Cell Adhesion Molecules - metabolism
Cell Movement - immunology
Cell Survival - immunology
Cells, Cultured
Dendritic Cells - cytology
Dendritic Cells - immunology
Immune System Phenomena - immunology
Immunoglobulin G - immunology
Immunoglobulins - deficiency
Immunoglobulins - genetics
Immunoglobulins - immunology
Immunoglobulins - metabolism
Immunologic Memory - immunology
Ligands
Mice
Mice, Inbred C57BL
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Summary: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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.0803892