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Immune events in skin. II. Inhibition of dendritic (veiled) cells function and traffic with anti-lymph dendritic cell
M I Dabrowski1, H Gałkowska, W L Olszewski
1Surgical Research and Transplantation Laboratory, Polish Academy of Sciences, Warsaw.
The migrating dendritic cells (DC) from the canine skin-draining afferent lymph are the most potent stimulators of the allogeneic MLR of all other lymph cell subpopulations. The MLR could be inhibited by addition of xenogeneic (rabbit), polyclonal anti-lymph dendritic cell serum (ADCS) to the cultures. ADCS blocked the presentation of Ia and CD1 antigens on the surface of DC. Studies using mouse anti-human monoclonal antibodies, cross-reactive with canine cells, indicate that blocking of Ia, but not of CD1 antigen, is responsible for inhibition of MLR. ADCS abrogated also the accessory function of DC in the lymph lymphocytes response to PHA. The inhibition reached 73%, when the serum was added for the whole period of the culture, and 23% after preincubation of DC with ADCS (anti-dendritic cell serum). ADCS administered subcutaneously into the dorsal area of hind paws caused a selective, transient disappearance of DC from the afferent lymph of normal dogs, which lasted for 2 h after the injection. We conclude, that the functional and physical elimination of migrating skin DC mediated by ADCS in vitro and in vivo, justify the possible use of this serum in the combined immunotherapy directed at the prolongation of skin graft survival.
The migrating dendritic cells (DC) from the canine skin-draining afferent lymph are the most potent stimulators of the allogeneic MLR of all other lymph cell subpopulations. The MLR could be inhibited by addition of xenogeneic (rabbit), polyclonal anti-lymph dendritic cell serum (ADCS) to the cultures. ADCS blocked the presentation of Ia and CD1 antigens on the surface of DC. Studies using mouse anti-human monoclonal antibodies, cross-reactive with canine cells, indicate that blocking of Ia, but not of CD1 antigen, is responsible for inhibition of MLR. ADCS abrogated also the accessory function of DC in the lymph lymphocytes response to PHA. The inhibition reached 73%, when the serum was added for the whole period of the culture, and 23% after preincubation of DC with ADCS (anti-dendritic cell serum). ADCS administered subcutaneously into the dorsal area of hind paws caused a selective, transient disappearance of DC from the afferent lymph of normal dogs, which lasted for 2 h after the injection. We conclude, that the functional and physical elimination of migrating skin DC mediated by ADCS in vitro and in vivo, justify the possible use of this serum in the combined immunotherapy directed at the prolongation of skin graft survival.