02077nas a2200253   4500000000100000008004100001260001300042653002400055653001100079653001100090653001200101653001600113653002500129653002200154653001800176100001500194700001500209700001500224245007400239300001100313490000700324520147800331022001401809       1987                            d  c1987 Mar10aAntigens, Bacterial10aBiopsy10aHumans10aleprosy10aMacrophages10aMycobacterium leprae10aPeripheral nerves10aSchwann Cells1 aRidley M J1 aWaters M F1 aRidley D S00aEvents surrounding the recognition of Mycobacterium leprae in nerves.  a99-1080 v553 a<p>Histological examination and immunocytochemistry of Schwann cells, macrophages, and mycobacterial antigen were used to study 48 nerves of untreated patients with leprosy. None of the patients was in reaction clinically, but microreactions, involving small clusters of Schwann cells and macrophages in all cases except LL, were marked by progressive degradation of acid-fast bacilli (AFB). This was thought to be the response to the recognition of mycobacterial antigen. In the first phase, the disintegration of one or more Schwann cells caused the release of AFB, accompanied by subacute inflammation. In the second phase, as edema and cellular infiltration subsided, the necrosis of Schwann cells was replaced by granuloma formation, mycobacterial antigen being in a soluble form. Myelinated cells harbored few degraded AFB, and there was evidence that antigen-associated myelin hastened the death of Schwann cells. Only then did antigen become immunologically detectable to induce an inflammatory response whose clearance and resolution was impeded by the restraint on cellular movement due to the structure of neural tissue. These developments were sporadic but continuous. AFB and antigen released by disintegrating Schwann cells were ingested by regenerating Schwann cells and by macrophages, producing a self-perpetuating cycle which might involve either small areas or the greater part of a fascicle, and could conceivably progress to a generalized reaction.</p>  a0148-916X