01904nas a2200325   4500000000100000008004100001260001300042653001200055653002300067653002000090653003000110653001700140653002600157653001200183653001600195653001400211653001700225653002500242653001300267653001800280653001100298100001200309700001400321700001400335245011700349300001100466490000700477520108000484022001401564       1989                            d  c1989 Apr10aAnimals10aCell Communication10aCells, Cultured10aCytotoxicity, Immunologic10aImmunization10aKiller Factors, Yeast10aleprosy10aLymphocytes10aNeuroglia10aPhagocytosis10aProtein Biosynthesis10aProteins10aSchwann Cells10aSpleen1 aMehta R1 aBirdi T J1 aAntia N H00aEffect of Mycobacterium leprae-infected Schwann cells and their supernatant on lymphocyte neuroglia interaction.  a149-550 v223 a<p>Since the resolution of neural lesions and subsequent nerve damage in leprosy must inevitably involve the participation of immune cells sensitized to Mycobacteria, we have used the dissociated Schwann cell culture model to study the relationship between M. leprae-infected Schwann cells and sensitized immune cells. Our earlier study on light and ultrastructural observations showed that on infection with M. leprae, the cytomorphology of Schwann cells remains unaffected, while degenerative changes suggestive of apoptosis are seen in extraneous lymphocytes which are subsequently phagocytosed by the Schwann cells. We now present additional evidence confirming that the phagocytosis of splenic cells by Schwann cells is indeed a two-step process. The first involves M. leprae-dependent cytotoxicity to splenic cells. This is followed by phagocytosis of these cells, which is a secondary and M. leprae-independent phenomenon. This finding has implications particularly on the weak inflammatory response observed in nerve lesions of a majority of lepromatous patients.</p>  a0165-5728