@article{2881,
  keywords = {Adolescent, Adult, Antigens, CD1, Biopsy, CD3 Complex, CD8 Antigens, Female, Humans, Hypersensitivity, Delayed, Immunohistochemistry, Ki-67 Antigen, leprosy, Male, Middle Aged, Mycobacterium leprae, Neuritis, Tuberculin Test, Wound Healing},
  author = {Siddiqui RM and Moreira A and Negesse Y and Taye G and Hanekom W and Haslett P and Britton S and Kaplan G},
  title = {Local nerve damage in leprosy does not lead to an impaired cellular immune response or decreased wound healing in the skin.},
  abstract = {<p>This study investigated whether peripheral nerve damage in patients with leprosy impairs local cellular immune responses, thereby reducing wound healing and leading to chronic skin ulceration. Anesthetic and contralateral sensitive skin sites in 42 patients with leprosy were compared for delayed-type hypersensitivity responses to purified protein derivative (PPD) of tuberculin. Leukocyte recruitment, epidermal activation, keratinocyte proliferation, and rates of wound healing after skin biopsy were compared. No significant differences in PPD-induced induration, epidermal activation and thickening or numbers of total T cells, CD8+ T cells, CD1a+ Langerhans cells, and proliferating Ki67+ keratinocytes were observed between anesthetic and sensitive skin sites. Similarly, rates of wound healing over 5 days after skin biopsy did not differ significantly. Thus, local leprosy-associated anesthesia does not appear to contribute to local immune compromise or impaired wound healing. Rather, chronic cutaneous ulceration in leprosy most likely results from repeated trauma associated with loss of sensation.</p>},
  year = {2002},
  journal = {The Journal of infectious diseases},
  volume = {186},
  pages = {260-5},
  month = {2002 Jul 15},
  issn = {0022-1899},
  doi = {10.1086/341204},
  language = {eng},
}