03338nas a2200457   4500000000100000008004100001260001300042653001500055653001000070653000900080653002200089653002600111653002400137653002300161653001000184653002100194653001100215653001100226653002100237653001200258653000900270653001600279653002500295653003100320653003100351653001700382100001400399700001200413700001600425700001200441700001100453700001200464700001700476700001800493245014300511856007800654300001000732490000800742520211600750022001402866       1998                            d  c1998 Jan10aAdolescent10aAdult10aAged10aAged, 80 and over10aAntibodies, Bacterial10aAntigens, Bacterial10aBacterial Proteins10aChild10aChild, Preschool10aFemale10aHumans10aImmunoglobulin G10aleprosy10aMale10aMiddle Aged10aMycobacterium leprae10aMycobacterium tuberculosis10aPolysaccharides, Bacterial10aTuberculosis1 aSousa A O1 aHenry S1 aMarója F M1 aLee F K1 aBrum L1 aSingh M1 aLagrange P H1 aAucouturier P00aIgG subclass distribution of antibody responses to protein and polysaccharide mycobacterial antigens in leprosy and tuberculosis patients.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1904868/pdf/cei0111-0048.pdf  a48-550 v1113 a<p>Immunoenzymatic assays were developed for the measurement of antibodies against mycobacterial lipoarabinomannan (LAM), a cell-free proteic extract (CFX) of Mycobacterium leprae, and the 38-kD protein antigen of M. tuberculosis. Sera from 108 leprosy patients, belonging to all clinical-immunological forms of the spectrum, and 81 patients with localized or disseminated tuberculosis (TB) were tested for antibodies of the four IgG subclasses. Standard calibration curves were used to allow comparisons between results of different isotypes and specificities. Mean concentrations of total IgG antibodies were higher in the overall leprosy population than in TB patients. In leprosy, levels of anti-CFX increased from tuberculoid toward lepromatous forms, with a clear switch from IgG1 to IgG2 subclass predominance. A similar IgG1 to IgG2 conversion was observed in anti-LAM antibodies, although total levels of anti-LAM were similar in patients with tuberculoid and lepromatous forms. In TB, antibodies against polysaccharide and protein antigens were both predominantly of IgG1 subclass, whatever the patient's clinical status, although lower in disseminated forms, probably due to concomitant HIV infection. A hypergammaglobulinaemia was also found in most leprosy and TB patients. In TB this was due to increased IgG1 and IgG3, especially in HIV co-infected patients. Based on the current knowledge of the influence of T cell-secreted cytokines on human immunoglobulin isotype expression, these results do not fit with a putative role of Th1 (such as found in TB and tuberculoid leprosy (TT)) and Th2 (such as found in leprosy lepromatous (LL) leprosy) environment in the isotypy of antibody responses in mycobacterial infections. Nor do variations of isotypy according to pathological conditions seem to be related to the biochemical nature of antigens, since antibodies to LAM and protein antigens had comparable evolutions of their subclass distribution. Other factors are to be investigated in order to understand better the significance and possible roles of antibodies in mycobacterial diseases.</p>  a0009-9104