Adaptive immune response in JAM-C-deficient mice: normal initiation but reduced IgG memory

Area of Science:

• Immunology
• Cell Biology
• Molecular Biology

Background:

• Junctional adhesion molecule C (JAM-C) deficient mice exhibit leukocytic pulmonary infiltrates, neutrophil homeostasis disruption, and increased mortality.
• Partial rescue in ventilated isolators suggests impaired ability to combat opportunistic infections.

Purpose of the Study:

• To investigate the adaptive immune responses in JAM-C deficient mice.
• To elucidate the role of JAM-C in dendritic cell function and adaptive immunity.

Main Methods:

• In vitro adhesion assays using murine dendritic cells (DCs) and recombinant JAM-C.
• Analysis of adaptive immune responses in JAM-C(-/-) mice upon protein antigen immunization and boosting.
• Assessment of antibody titers in a model of antigen-induced arthritis.

Main Results:

• Murine conventional dendritic cells express JAM-B, a ligand for JAM-C, and can interact via Mac-1.
• JAM-C interaction via Mac-1 is not essential for dendritic cell migration or function in vivo.
• JAM-C deficient mice show reduced persistence of specific circulating antibodies after immunization and boosting.
• Specific IgG2a antibody titers are reduced in JAM-C deficient mice compared to wild-type controls.

Conclusions:

• JAM-C deficiency impacts the adaptive humoral immune response, specifically affecting antibody persistence.
• The findings suggest a role for JAM-C in adaptive immunity beyond its previously observed role in innate immunity.