mAb against junctional adhesion molecule C (JAM-C)—involved in leukocyte migration through the endothelium—were reported to increase the Th1 response leading to reduced skin lesions and parasite burden in resistant C57BL/6 mice, while it boosted the Th2 response promoting infection in susceptible BALB/c mice (20). The gene discussed is JAM3; the disease is infection.