Changes in the cellular immune response by a subfraction of burned murine skin.
Sepsis due to impaired host defence mechanisms is one of the most frequent causes of death in severely burned patients. However, it is not precisely known to what extent syntheses and release of suppressive mediators of the burned tissue affect the cellular and humoral immune responses. In this study a decreased production of plasminogen activator by macrophages is demonstrated after incubation with skin components, indicating a decreased macrophage helper function for T-B cell cooperation. An additional effect of the skin fraction is a considerable increase in mitogenic activity as measured in the antibody-forming cell test. This enhancement of macrophage-T-B cell cooperation is concentration dependent and lower in the burned skin fraction as compared to the unburned control. A known skin-derived cytokine with mitogenic properties is epidermal cell-derived thymocyte activating factor (ETAF) exhibiting interleukin-1 (I1-1) like activity including mitogenic enhancement of murine thymocyte stimulation by phytohaemagglutinin. Burned and control skin fraction as tested in a thymocyte assay did not show interleukin-1-like activity. The experiments suggest the presence of a skin-derived growth factor which is not interleukin-1 but which stimulates T-B cell cooperation when there is depression of macrophage function. Further purification is required in order to assess the clinical relevance of the factor in burned patients.
D000818:Animals; D000917:Antibody Formation; D002056:Burns / Q000276:immunology*; D005260:Female; D007111:Immunity, Cellular; D007376:Interleukin-2 / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D008815:Mice, Inbred Strains; D010960:Plasminogen Activators / Q000276:immunology; D012867:Skin / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D007376:Interleukin-2; D010960:Plasminogen Activators