Kinetics of humoral responsiveness in severe thermal injury.
Severe thermal injury has the capacity to increase the rate of generation of antibody-forming cells in mice. The intensity of stimulation appears to be proportional to the extent of injury. The effect has been observed in animals burned within 1 hr before or after sensitization with test antigen(s), and persists up to 14 days after injury. Thereafter, the stimulatory effect wanes, and disappears by the 21st day after burning. Responses to T-cell (thymus derived lymphocytes) dependent antigens (sheep erythrocytes; sheep erythrocytes coupled to TNP) and to antigens not requiring T and B-cell (bone marrow derived lymphocytes) cooperation (DNP-Ficoll) appear to be equally affected by thermal injury. The mechanisms underlying this form of enhanced antibody response are not clear. The data, however, support the possibility that the burn wound may release factor(s) capable of enhancing humoral responsiveness in the injured animal. Such factor(s) do not appear to be endotoxins.
D000818:Animals; D000917:Antibody Formation; D000921:Antibody-Producing Cells; D002056:Burns / Q000276:immunology*; D004912:Erythrocytes / Q000276:immunology; D007114:Immunization; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009596:Nitrophenols / Q000276:immunology; D012756:Sheep; D012772:Shock, Septic / Q000276:immunology; D013154:Spleen / Q000276:immunology
D009596:Nitrophenols