02011nas a2200265   4500000000100000008004100001260001700042653001200059653001400071653001400085653002400099653001100123653001200134653002500146653001800171653002800189653001800217100001300235245004800248300001000296490000700306050003200313520138600345022001401731       1996                            d  c1996 Jan-Mar10aAnimals10aCytokines10aGranuloma10aHeat-Shock Proteins10aHumans10aleprosy10aMycobacterium leprae10aMyelin Sheath10aNervous System Diseases10aSchwann Cells1 aTurk J L00aHost parasite response in nerve in leprosy.  a113-70 v68  aInfolep Library - available3 a<p>Nerve granulomas occur at all points across the leprosy spectrum. Studies have been made using experimental models in which mycobacteria were injected directly in the sciatic or posterior tibial nerve of the guinea pig. Clinical and electrophysiological studies demonstrated axonal damage which was confirmed by morphometric studies showing disrupted myelin sheaths and in places complete demyelination. Further immunohistological studies showed a complete disappearance of staining for certain neuropeptides. The role of Schwann cells has also been investigated. Schwann cells in nerves affected by mycobacterial granulomas, both experimental and in leprosy patients were not demonstrated to be MHC class II positive suggesting that they did not play a role in antigen presentation. Macrophages in leprosy granulomas were shown to contain TNF alpha, suggesting that this cytokine played a role in axonal damage. The role of mycobacterial heat-shock protein in nerve granulomas has not as yet been determined. The localized nature of granulomas in leprosy nerves and nerves with experimental mycobacterial granulomas has been studied by a process of excision and repair with muscle grafts. Marked recovery has been demonstrated by clinical, electrophysiological, morphometric and immuno-histochemical techniques, the latter demonstrating a return of neuropeptide production.</p>  a0254-9395