The experimental granuloma. A hypothesis to explain the persistence of the lesion.
Granulomatous inflammation is the morphological substrate of a variety of important infectious diseases such as tuberculosis, leprosy, schistosomiasis and others. Nevertheless, although many aspects of this special type of inflammation are known, fundamental questions concerning granuloma formation, persistence, fate and significance for host-parasite relationships still remain to be elucidated. In this brief review, the basic and more relevant literature related to experimental investigations on granuloma physiopathology is presented. Based on recent investigations performed in our laboratory showing that MDF (Macrophage Deactivating Factor) secreted by epithelioid cells and characterized as the calcium-binding protein protein MRP-14 deactivates activated macrophages, a hypothesis to explain the persistence of granulomatous inflammation is put forward.
D000818:Animals; D000943:Antigens, Differentiation / Q000502:physiology; D002135:Calcium-Binding Proteins / Q000502:physiology; D040501:Calgranulin A; D040502:Calgranulin B; D002464:Cell Migration Inhibition; D015622:Epithelioid Cells / Q000502:physiology; D006099:Granuloma / Q000276:immunology / Q000473:pathology*; D006801:Humans; D015441:Leprosy, Tuberculoid / Q000473:pathology; D008263:Macrophage Migration-Inhibitory Factors; D008264:Macrophages / Q000473:pathology*; D051379:Mice
D000943:Antigens, Differentiation; D002135:Calcium-Binding Proteins; D040501:Calgranulin A; D040502:Calgranulin B; D008263:Macrophage Migration-Inhibitory Factors