02069nas a2200301   4500000000100000008004100001260000900042653001500051653001000066653002700076653002400103653001100127653001100138653002800149653001200177653000900189653001600198653002500214653002200239100001500261700001600276700001400292245017000306300001000476490000700486520126000493022001401753       1994                            d  c199410aAdolescent10aAdult10aAntibodies, Monoclonal10aAntigens, Bacterial10aFemale10aHumans10aImmunoenzyme Techniques10aleprosy10aMale10aMiddle Aged10aMycobacterium leprae10aPeripheral nerves1 aShetty V P1 aUplekar M W1 aAntia N H00aImmunohistological localization of mycobacterial antigens within the peripheral nerves of treated leprosy patients and their significance to nerve damage in leprosy.  a300-60 v883 a<p>The presence and distribution of Mycobacterium leprae-specific and cross-reacting antigens within the peripheral nerves of multidrug-treated patients with leprosy was investigated to gain a better understanding of the mechanism of nerve damage and the effect of multidrug therapy (MDT) on it. There was no specific qualitative difference in the type of antigens in the leprosy spectrum. However, our results indicate that there may be differential handling of antigens by the macrophages as compared to Schwann cells. This could play a key role in the pathogenesis of the disease. Multidrug treatment is effective in arresting the progression of the disease process as well as in reducing the viable bacterial load, both in borderline lepromatous and lepromatous (MB) and borderline tuberculoid and tuberculoid (PB) cases. However, the presence of M. leprae antigens in all the multidrug-treated MB nerve lesions and 87% of PB nerve lesions suggest that the antigens persist for a prolonged period. Hence, the risk of immunological reaction and antigen-associated silent nerve damage may continue even after majority of M. leprae were killed. The findings give further support to the view that most of the nerve damage is due to bacterial antigens.</p>  a0001-6322