@article{7392,
  keywords = {Adult, Aged, Antigens, Differentiation, T-Lymphocyte, Antigens, Neoplasm, Female, Flow Cytometry, Humans, Immunity, Cellular, leprosy, Leprosy, lepromatous, Leprosy, Tuberculoid, Male, Membrane Glycoproteins, Middle Aged, Receptors, Lymphocyte Homing, T-Lymphocyte Subsets, Up-Regulation},
  author = {Sieling PA and Legaspi A and Ochoa MT and Rea T and Modlin RL},
  title = {Regulation of human T-cell homing receptor expression in cutaneous bacterial infection.},
  abstract = {<p>We investigated the regulation of T-cell homing receptors in infectious disease by evaluating the cutaneous lymphocyte antigen (CLA) in human leprosy. We found that CLA-positive cells were enriched in the infectious lesions associated with restricting the growth of the pathogen Mycobacterium leprae, as assessed by the clinical course of infection. Moreover, CLA expression on T cells isolated from the peripheral blood of antigen-responsive tuberculoid leprosy patients increased in the presence of M. leprae (2.4-fold median increase; range 0.8-6.1, n = 17), but not in unresponsive lepromatous leprosy patients (1.0-fold median increase; range 0.1-2.2, n = 10; P < 0.005). Mycobacterium leprae specifically up-regulated the skin homing receptor, CLA, but not alpha(4)/beta(7), the intestinal homing receptor, which decreased on T cells of patients with tuberculoid leprosy after antigen stimulation (2.2-fold median decrease; range 1.6-3.4, n = 3). Our data indicate that CLA expression is regulated during the course of leprosy infection and suggest that T-cell responsiveness to a microbial antigen directs antigen-specific T cells to the site of infection.</p>},
  year = {2007},
  journal = {Immunology},
  volume = {120},
  pages = {518-25},
  month = {2007 Apr},
  issn = {0019-2805},
  url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2265905/pdf/imm0120-0518.pdf},
  doi = {10.1111/j.1365-2567.2006.02528.x},
  language = {eng},
}