![]() Mac-2+ M phi dramatically enhanced alloreactivity at low concentrations with normal host Mac-2+ M phi providing greater enhancement of alloreactivity than TBH Mac-2+ M phi. Indomethacin treatment did reduce suppression mediated by Mac-2+, -3+, and unsorted M phi. Indomethacin treatment did not effect the suppression caused by Mac-1+ M phi, suggesting that proataglandin E2 was not involved. There were no differences in the suppression caused by normal or TBH Mac-2+ M phi, and by normal or TBH Mac-3+ M phi. TBH Mac-1+ reduced alloreactivity by 31% and 59% at low and high concentrations, respectively. When separated into subpopulations, normal host Mac-1+ M phi reduced alloreactivity by 48% and 81% when added at low and high concentrations, respectively. ![]() Unsorted TBH M phi reduced alloreactivity by 64% and 86% at low and high concentrations, respectively. Suppression reached 68% when high concentrations of unsorted normal host M phi were added to the MLR cultures. The low concentration of unsorted normal host M phi caused a 31% suppression of alloreactivity. Both M phi types were added to mixed lymphocyte reaction (MLR) cultures at concentrations ranging from a low of 2% M phi to a high of 20% M phi. The separated Mac-1+, -2+, and -3+ M phi were called sorted M phi, while unseparated M phi were designated unsorted M phi. To measure the accessory activity of M phi for T cell alloreactivity, thioglycollate-elicited peritoneal M phi from normal and tumor-bearing hosts (TBH) were labeled with anti-Mac-1, -2, or -3 antibodies and separated by flow cytofluorometry. Our studies of tumor-induced M phi-mediated dysfunction used M phi subsets which were defined by their Mac-1, Mac-2, and Mac-3 surface markers. Macrophages (M phi) are multifunctional cells that regulate humoral and cellular immune responses.
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