@article{11355,
  keywords = {Antibodies, Bacterial, Antigens, Bacterial, B-Lymphocytes, Female, Glycolipids, Humans, Immunoglobulin G, Immunoglobulin M, Lepromin, leprosy, Longitudinal studies, Lymphocyte Activation, Male, Mycobacterium leprae, T-Lymphocytes},
  author = {Koster F T and Scollard D M and Umland E T and Fishbein D B and Hanly W C and Brennan P J and Nelson K E},
  title = {Cellular and humoral immune response to a phenolic glycolipid antigen (PhenGL-I) in patients with leprosy.},
  abstract = {<p>The ability of phenolic glycolipid I (PhenGL-I) of Mycobacterium leprae to stimulate in vitro lymphocyte proliferation (LP) was tested in cultures of peripheral blood cells from 42 patients with leprosy in Chicago and Thailand, 9 individuals with household contact in Thailand, and 10 unexposed North American controls. Only 10 responders (24%) were found among the patients, and the degree of LP was small. Responders were found among patients with lepromatous (18%) or tuberculoid (30%) leprosy without relation to age, complications, duration of treatment, or lepromin responsiveness. The specificity of the response was supported by a lack of response to two other glycolipids, by responses by T cells but not B cells, and by the observation that three of four responders tested maintained their responses to PhenGL-I for at least 1 year. Serum immunoglobulin M (IgM) and IgG antibodies were measured in the same patients by using PhenGL-I or its terminal monosaccharide conjugated to a bovine serum albumin carrier in an enzyme-linked immunosorbent assay. The presence of IgM antibody correlated negatively with LP to lepromin and to PhenGL-I in patients with tuberculoid leprosy. We conclude that circulating T cells from some leprosy patients proliferate in the presence of PhenGL-I in vitro, but the response is weak, possibly due to concomitant suppression or inhibition. The predominance of IgM antibody to PhenGL-I may be related to a lack of a T-helper-cell-mediated switch to IgG antibody response.</p>},
  year = {1987},
  journal = {Journal of clinical microbiology},
  volume = {25},
  pages = {551-6},
  month = {1987 Mar},
  issn = {0095-1137},
  url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC265987/pdf/jcm00087-0107.pdf},
  language = {eng},
}