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The viewpoints on the control of innate immune cells by the adaptive immunesystem during sepsis remain controversial. Mitogen-activated protein kinase phosphatase-1(MKP-1) is essential to the negative control of innate immunity and suppressesthe activation of macrophages by inhibiting activated mitogen-activated proteinkinase (MAPK). The purpose of the current study was to observe inflammatory responseand macrophage activation in mice with severe combined immunodeficiency (SCID)with endotoxemia and to determine the role of MKP-1 in the control of macrophageactivation by the adaptive immune system. Endotoxemia was induced in wild-typeand SCID mice by an intraperitoneal injection of lipopolysaccharide (LPS), andall of the SCID mice died. SCID mice produced more inflammatory cytokines thanBALB/c mice systemically and locally. TNF-α mRNA expression was higher and MKP-1mRNA expression was lower in peritoneal macrophages (PMa) from SCID mice comparedto PMa from wild-type mice after and even before LPS injection. Thioglycollate-stimulatedPMa from wild-type mice were stimulated with LPS in vitro in the presence or absenceof pan-T cells. The levels of TNF-α and IL-6 were higher in the supernatants fromPMa cultured alone compared to PMa co-cultured with pan-T cells, and PMa MKP-1mRNA and protein expression were higher when PMa were co-cultured with pan-T cells.Therefore, pan-T cells can up-regulate MKP-1 expression in macrophages and inhibitthe secretion of inflammatory cytokines secretion by macrophages. In SCID mice,lymphocyte deficiency, especially T cell deficiency, causes insufficient MKP-1expression in macrophages, which can be responsible for the severe inflammationand bad prognosis of septic SCID mice. MKP-1 plays an important role in the controlof macrophage activation by the adaptive immune system.

Mitogen-activated protein kinase phosphatase-1 expression in macrophages is controlled by lymphocytes during macrophage activation