ArticleInfection and immunity1995
Immunoglobulin G1 (IgG1) and IgG3 antibodies are markers of progressive disease in leprosy.
Article in Infection and immunity, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Alteration of Endocrine Hormones and Antibody Responses in Different Spectrum of Tuberculosis Disease.Frontiers in immunology · 2022Article
- Utility of immunoglobulin isotypes against LID-1 and NDO-LID for, particularly IgG1, confirming the diagnosis of multibacillary leprosy.Memorias do Instituto Oswaldo Cruz · 2018Article
- IgG1 deficiency exacerbates experimental autoimmune myasthenia gravis in BALB/c mice.Journal of neuroimmunology · 2015Article
- Dynamics of the interaction of human IgG subtype immune complexes with cells expressing R and H allelic forms of a low-affinity Fc gamma receptor CD32A.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- T-cell and serological responses to Erp, an exported Mycobacterium tuberculosis protein, in tuberculosis patients and healthy individuals.BMC infectious diseases · 2007Article
- IgG1 antimycobacterial antibodies can reverse the inhibitory effect of pentoxifylline on tumour necrosis factor alpha (TNF-alpha) secreted by mycobacterial antigen-stimulated adherent cells.Clinical and experimental immunology · 2004Article
- Article
- Effects of anti-endothelial cell antibodies in leprosy and malaria.Infection and immunity · 2004Article
- IgG subclass response to Helicobacter pylori and CagA antigens in children.Clinical and experimental immunology · 2003Article
- Differential changes in heat shock protein-, lipoarabinomannan-, and purified protein derivative-specific immunoglobulin G1 and G2 isotype responses during bovine Mycobacterium avium subsp. paratuberculosis infection.Infection and immunity · 2001Article
- Opsonizing antibodies (IgG1) up-regulate monocyte proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and IL-6 but not anti-inflammatory cytokine IL-10 in mycobacterial antigen-stimulated monocytes-implications for pathogenesis.Clinical and experimental immunology · 2001Article
- PPD-specific IgG1 antibody subclass upregulate tumour necrosis factor expression in PPD-stimulated monocytes: possible link with disease pathogenesis in tuberculosis.Clinical and experimental immunology · 2000Article
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- Immunoglobulin subclass distribution and diagnostic value of Leishmania donovani antigen-specific immunoglobulin G3 in Indian kala-azar patients.Clinical and diagnostic laboratory immunology · 1999Article
- Increases in the levels of Coxiella burnetii-specific immunoglobulin G1 and G3 antibodies in acute Q fever and chronic Q fever.Clinical and diagnostic laboratory immunology · 1998Article
- IgG subclass distribution of antibody responses to protein and polysaccharide mycobacterial antigens in leprosy and tuberculosis patients.Clinical and experimental immunology · 1998Article
- Selective increases in antibody isotypes and immunoglobulin G subclass responses to secreted antigens in tuberculosis patients and healthy household contacts of the patients.Clinical and diagnostic laboratory immunology · 1995Article
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium leprae-specific and polyclonal immunoglobulin G (IgG) subclass and IgE antibodies in leprosy patients across the histopathological spectrum were determined by using a quantitative enzyme-linked immunosorbent assay. Antibody responses to M. leprae sonicates were detected only in IgG1, -2, and -3 subclasses. Even at 100-times-lower dilutions, very little IgG4 and IgE antibody activity against M. leprae was detected in any group of leprosy patients. Quantitatively, antibody responses were highest at the lepromatous pole and decreased towards the tuberculoid pole. The greatest quantitative difference in antibodies between the lepromatous and tuberculoid poles was observed with IgG1 (140-fold), this was followed by the difference with IgG3 antibodies (32-fold). Polyclonal antibodies, on the other hand, were elevated for all four IgG subclasses as well as IgE in both lepromatous and tuberculoid leprosy patients compared with healthy controls from a leprosy-endemic area. Selective elevation of M. leprae-specific antibody responses in IgG1 and IgG3 subclasses, therefore, could not be attributed to selective polyclonal activation in these particular subclasses. Furthermore, polyclonal activation for IgE was observed in both lepromatous and tuberculoid leprosy patients, with higher levels in the tuberculoid group, which does not support selective TH2 activation in lepromatous leprosy patients. IgG1 and IgG3 antibodies also showed the highest Spearman rank correlation with the bacterial index in these patients (rho = 0.748 and P < 0.001 for IgG1; rho = 0.721 and and P < 0.001 for IgG3). Thus, disease progression in leprosy showed a significant correlation with selective increases in IgG1 and IgG3 responses.
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