Additionally, the lack of involvement of the MAPK p38 and ERK 1/2 pathways in IFN-γ production in infected CBA murine cells stimulated with the two secreted/excreted antigens, considered in conjunction with the production of IL-4 showing involvement only via the ERK 2 pathway under stimulation by SeT1 antigen during 60-day infection period with the virulent strain, suggests that these signaling pathways may cooperate to regulate the production of only pro-inflammatory and regulatory cytokines in the splenic cells of CBA mice. The gene discussed is IL4; the disease is infection.