Mechanisms controlling differentiation and function of antigen-presenting macrophages.
We have briefly reviewed our studies on the mechanisms controlling the differentiation and activation of peritoneal antigen-presenting cells. We demonstrated that the peritoneal population is composed of two main subsets of cells, only one of which participates actively in primary antigen presentation. The latter is missing in athymic mice and seems to differentiate under the influence of the shortlived, cortisone-resistant subpopulation of thymocytes. The maturation of the peritoneal macrophages is subjected also to an additional inducing effect, that of the spleen. Macrophages from splenectomized donors are impaired both with respect to antigen presentation to naive and to primed lymphocytes, and with respect to phagocytosis of "opsonized" bacteria. The mature antigen-presenting cell is subjected to activating signals deriving from the Fc-bound Ig molecule. This is mediated via a tetrapeptide, tuftsin, which is cleaved off the CH2 portion of the Ig and activates the immunogenic effect of the antigen-pulsed macrophage.
D000818:Animals; D000941:Antigens / Q000276:immunology*; D002454:Cell Differentiation; D008214:Lymphocytes / Q000276:immunology; D008262:Macrophage Activation; D008264:Macrophages / Q000187:drug effects / Q000276:immunology* / Q000528:radiation effects; D051379:Mice; D008819:Mice, Nude; D011961:Receptors, Fc / Q000032:analysis; D013154:Spleen / Q000276:immunology; D013156:Splenectomy; D013601:T-Lymphocytes / Q000276:immunology; D013950:Thymus Gland / Q000276:immunology; D014405:Tuftsin / Q000494:pharmacology
D000941:Antigens; D011961:Receptors, Fc; D014405:Tuftsin