ArticleInfection and immunity1999
Differential decline in Leishmania membrane antigen-specific immunoglobulin G (IgG), IgM, IgE, and IgG subclass antibodies in Indian kala-azar patients after chemotherapy.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Systematic review on antigens for serodiagnosis of visceral leishmaniasis, with a focus on East Africa.PLoS neglected tropical diseases · 2019Pooled it
- Systematic review of biomarkers to monitor therapeutic response in leishmaniasis.Antimicrobial agents and chemotherapy · 2015Pooled it
- Detection of anti-leishmania (Leishmania) chagasi immunoglobulin G by flow cytometry for cure assessment following chemotherapeutic treatment of American visceral leishmaniasis.Clinical and vaccine immunology : CVI · 2007Trial
- Humoral response in Leishmaniasis.Frontiers in cellular and infection microbiology · 2022Review
- Wnt5A Signaling Blocks Progression of Experimental Visceral Leishmaniasis.Frontiers in immunology · 2022Article
- Potential biomarkers of immune protection in human leishmaniasis.Medical microbiology and immunology · 2021Review
- Effect of Prophylactic Vaccination with the Membrane-Bound Acid Phosphatase Gene ofJournal of immunology research · 2021Article
- High levels of serum glycans monovalent IgG immune complexes detected by dissociative ELISA in experimental visceral leishmaniasis.Immunology · 2019Article
- Preclinical diagnosis of American visceral leishmaniasis during early onset of human Leishmania (L.) infantum chagasi-infection.Pathogens and global health · 2014Article
- IgG1 as a potential biomarker of post-chemotherapeutic relapse in visceral leishmaniasis, and adaptation to a rapid diagnostic test.PLoS neglected tropical diseases · 2014Article
- Deficiency of p110δ isoform of the phosphoinositide 3 kinase leads to enhanced resistance to Leishmania donovani.PLoS neglected tropical diseases · 2014Article
- Vaccine Development Against Leishmania donovani.Frontiers in immunology · 2012Article
- Murine visceral leishmaniasis: IgM and polyclonal B-cell activation lead to disease exacerbation.European journal of immunology · 2010Article
- Inaccuracy of enzyme-linked immunosorbent assay using soluble and recombinant antigens to detect asymptomatic infection by Leishmania infantum.PLoS neglected tropical diseases · 2009Article
- Immune response regulation by leishmania secreted and nonsecreted antigens.Journal of biomedicine & biotechnology · 2007Article
- Leishmania promastigote membrane antigen-based enzyme-linked immunosorbent assay and immunoblotting for differential diagnosis of Indian post-kala-azar dermal leishmaniasis.Journal of clinical microbiology · 2005Article
- Characterization of immunoglobulin G and its subclass response to Indian kala-azar infection before and after chemotherapy.Infection and immunity · 2004Article
- Immunoglobulin E antileishmanial antibody response in cutaneous leishmaniasis.Clinical and diagnostic laboratory immunology · 2002Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathogenesis in kala-azar is associated with depressed cellular immunity and significant elevation of antileishmanial antibodies. Since these antibodies are present even after cure, analysis of the parasite-specific isotypes and immunoglobulin G (IgG) subclasses in kala-azar patients may shed new light on the immune responses during progression and resolution of infection. Using leishmanial membrane antigenic extracts, we investigated the relative levels of specific IgG, IgM, IgA, IgE, and IgG subclasses in Indian kala-azar patient sera during disease, drug resistance, and cure. Acute-phase sera showed strong stimulation of IgG, followed by IgE and IgM and lastly by IgA antibodies. IgG subclass analysis revealed expression of all of the subclasses, with a predominance of IgG1 during disease. Following sodium stibogluconate (SAG) resistance, the levels of IgG, IgM, IgE, and IgG4 remained constant, while there was a decrease in the titers of IgG2 and IgG3. In contrast, a significant (2.2-fold) increase in IgG1 was observed in these individuals. Cure, in both SAG-responsive and unresponsive patients, correlated with a decline in the levels of IgG, IgM, IgE, and all of the IgG subclasses. The stimulation of IgG1 and the persistence, most importantly, of IgE and IgG4 following drug resistance, along with a decline in IgE, IgG4, and IgG1 with cure, demonstrate the potential of these isotypes as possible markers for monitoring effective treatment in kala-azar.
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