Modification of in vitro and in vivo immune function by acute inflammatory cells.
The ability of adoptively transferred, syngeneic polymorphonuclear leukocyte-rich (PMNLr) inflammatory cells to influence lymphocyte-mediated cytotoxicity (LMC), complement-dependent cytotoxicity (CDC), and skin allograft survival was studied in a murine model. BALB/c mouse PMNLr, stimulated by i.p. injection of either glycogen (G/PMNLr) or thioglycollate (T/PMNLr), were transferred to other BALB/c mice at the time of primary or secondary immunization with a cellular alloantigen (C57BL/6 spleen cells) or after skin allografting (C57BL/6 tailskin). The metabolic activity of each PMNLr population was determined by measuring glucose utilization in the hexose monophosphate shunt. It appeared that metabolic activity of the T/PMNLr was significantly greater than that of the G/PMNLr. Our results indicate that, while the infusion of G/PMNLr tended to suppress the primary cell-mediated immune response and the secondary humoral immune response, the infusion of T/PMNLr stimulated both of these responses. Furthermore, i.p. infusion of mice with G/PMNLr at a time approximating grafting resulted in prolonged graft survival, but neither T/PMNLr nor syngeneic thymocytes effect graft survival. Our data demonstrate that both cellular and humoral immunity can be modified by acute inflammatory cells. The metabolic status of the acute inflammatory cells seems to be critical in determining their immunoregulatory potential.
D000818:Animals; D001803:Blood Transfusion; D003165:Complement System Proteins / Q000276:immunology*; D003602:Cytotoxicity, Immunologic; D006085:Graft Survival; D008214:Lymphocytes / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C / Q000276:immunology; D008810:Mice, Inbred C57BL / Q000276:immunology; D009504:Neutrophils / Q000276:immunology* / Q000637:transplantation; D016038:Skin Transplantation
D003165:Complement System Proteins