02581nas a2200397   4500000000100000008004100001260001300042653002600055653002400081653001800105653001100123653001600134653001100150653002100161653002100182653001300203653001200216653002500228653002600253653000900279653002500288653001800313100001500331700001700346700001500363700001700378700001400395700001600409700001500425245011100440856007800551300001000629490000700639520152300646022001402169       1987                            d  c1987 Mar10aAntibodies, Bacterial10aAntigens, Bacterial10aB-Lymphocytes10aFemale10aGlycolipids10aHumans10aImmunoglobulin G10aImmunoglobulin M10aLepromin10aleprosy10aLongitudinal studies10aLymphocyte Activation10aMale10aMycobacterium leprae10aT-Lymphocytes1 aKoster F T1 aScollard D M1 aUmland E T1 aFishbein D B1 aHanly W C1 aBrennan P J1 aNelson K E00aCellular and humoral immune response to a phenolic glycolipid antigen (PhenGL-I) in patients with leprosy.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC265987/pdf/jcm00087-0107.pdf  a551-60 v253 a<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>  a0095-1137