@article{3367,
  keywords = {Algorithms, Cluster Analysis, Colony Count, Microbial, Cytokines, Gene Expression Profiling, Gene Expression Regulation, Genes, Immunoglobulin, Humans, Immunity, Cellular, Immunity, Innate, Leprosy, lepromatous, Leprosy, Tuberculoid, Macrophages, Alveolar, Membrane Glycoproteins, Mycobacterium tuberculosis, Oligonucleotide Array Sequence Analysis, polymerase chain reaction, Principal Component Analysis, Receptors, Cell Surface, Receptors, Immunologic, Toll-Like Receptors, Up-Regulation},
  author = {Bleharski J and Li H and Meinken C and Graeber T and Ochoa M and Yamamura M and Burdick A and Sarno E and Wagner M and Röllinghoff M and Rea T and Colonna M and Stenger S and Bloom B and Eisenberg D and Modlin RL},
  title = {Use of genetic profiling in leprosy to discriminate clinical forms of the disease.},
  abstract = {<p>Leprosy presents as a clinical and immunological spectrum of disease. With the use of gene expression profiling, we observed that a distinction in gene expression correlates with and accurately classifies the clinical form of the disease. Genes belonging to the leukocyte immunoglobulin-like receptor (LIR) family were significantly up-regulated in lesions of lepromatous patients suffering from the disseminated form of the infection. In functional studies, LIR-7 suppressed innate host defense mechanisms by shifting monocyte production from interleukin-12 toward interleukin-10 and by blocking antimicrobial activity triggered by Toll-like receptors. Gene expression profiles may be useful in defining clinical forms of disease and providing insights into the regulation of immune responses to pathogens.</p>},
  year = {2003},
  journal = {Science (New York, N.Y.)},
  volume = {301},
  pages = {1527-30},
  month = {2003 Sep 12},
  issn = {1095-9203},
  doi = {10.1126/science.1087785},
  language = {eng},
}