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Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region
BACKGROUND: Infectious agents can activate self-reactive T cells. In general, infections trigger various mechanisms, including a lack of auto-tolerance, induction of costimulatory molecules on antigen presenting cells, and molecular simulation, in addition to cross-reactions between microbial antige...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452639/ https://www.ncbi.nlm.nih.gov/pubmed/28566085 http://dx.doi.org/10.1186/s40249-017-0294-2 |
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author | Bichara, Clea Nazaré Carneiro Bichara, Carlos David Araújo Tostes, Camila Povoa, Marinete Marins Quaresma, Juarez Antonio Simões Xavier, Marília Brasil |
author_facet | Bichara, Clea Nazaré Carneiro Bichara, Carlos David Araújo Tostes, Camila Povoa, Marinete Marins Quaresma, Juarez Antonio Simões Xavier, Marília Brasil |
author_sort | Bichara, Clea Nazaré Carneiro |
collection | PubMed |
description | BACKGROUND: Infectious agents can activate self-reactive T cells. In general, infections trigger various mechanisms, including a lack of auto-tolerance, induction of costimulatory molecules on antigen presenting cells, and molecular simulation, in addition to cross-reactions between microbial antigens and self-antigens. HIV and leprosy coinfections lead to self-immunity with the production of autoantibodies. However, not enough data on the immune behaviour associated with this coinfection are available. Therefore, this study focused on the detection of autoantibodies against cellular antigens (AACA) in individuals with HIV and leprosy coinfection in the Amazon region. METHODS: Patients were distributed into four groups according to their infections: (i) coinfection with HIV and leprosy (n = 23), (ii) infection with leprosy (n = 33), (iii) infection with HIV/AIDS (n = 25), and (iv) healthy blood donor controls (n = 100). AACA were identified by indirect immunofluorescence and the samples were tested using a commercial diagnosis kit containing the antinuclear antibody HEp-2. RESULTS: Morphologically, all stages of cell division were assessed in addition to the morphological features associated with the nuclear matrix, nucleolus, mitotic spindle, and cytoplasm. There was a high prevalence of AACA in the coinfection group (47.8%, n = 11) when compared with the control group of healthy blood donors (2.0%). The results showed predominantly cytoplasmic staining in all groups analysed, and no difference was observed between the presence or absence of AACA and the leprosy forms (paucibacillary and multibacillary) in the coinfection group. CONCLUSIONS: The results of this study show that despite the tendency of coinfected patients to have higher levels of autoantibodies, no correlation was observed between clinical and laboratorial variables and morbidity associated with HIV and leprosy coinfections or the levels of AACA in the serum of coinfected patients. These data are important to elucidate this complex relationship between HIV and leprosy and thus improve the follow-up of these patients. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40249-017-0294-2) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5452639 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-54526392017-06-02 Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region Bichara, Clea Nazaré Carneiro Bichara, Carlos David Araújo Tostes, Camila Povoa, Marinete Marins Quaresma, Juarez Antonio Simões Xavier, Marília Brasil Infect Dis Poverty Research Article BACKGROUND: Infectious agents can activate self-reactive T cells. In general, infections trigger various mechanisms, including a lack of auto-tolerance, induction of costimulatory molecules on antigen presenting cells, and molecular simulation, in addition to cross-reactions between microbial antigens and self-antigens. HIV and leprosy coinfections lead to self-immunity with the production of autoantibodies. However, not enough data on the immune behaviour associated with this coinfection are available. Therefore, this study focused on the detection of autoantibodies against cellular antigens (AACA) in individuals with HIV and leprosy coinfection in the Amazon region. METHODS: Patients were distributed into four groups according to their infections: (i) coinfection with HIV and leprosy (n = 23), (ii) infection with leprosy (n = 33), (iii) infection with HIV/AIDS (n = 25), and (iv) healthy blood donor controls (n = 100). AACA were identified by indirect immunofluorescence and the samples were tested using a commercial diagnosis kit containing the antinuclear antibody HEp-2. RESULTS: Morphologically, all stages of cell division were assessed in addition to the morphological features associated with the nuclear matrix, nucleolus, mitotic spindle, and cytoplasm. There was a high prevalence of AACA in the coinfection group (47.8%, n = 11) when compared with the control group of healthy blood donors (2.0%). The results showed predominantly cytoplasmic staining in all groups analysed, and no difference was observed between the presence or absence of AACA and the leprosy forms (paucibacillary and multibacillary) in the coinfection group. CONCLUSIONS: The results of this study show that despite the tendency of coinfected patients to have higher levels of autoantibodies, no correlation was observed between clinical and laboratorial variables and morbidity associated with HIV and leprosy coinfections or the levels of AACA in the serum of coinfected patients. These data are important to elucidate this complex relationship between HIV and leprosy and thus improve the follow-up of these patients. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40249-017-0294-2) contains supplementary material, which is available to authorized users. BioMed Central 2017-06-01 /pmc/articles/PMC5452639/ /pubmed/28566085 http://dx.doi.org/10.1186/s40249-017-0294-2 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Bichara, Clea Nazaré Carneiro Bichara, Carlos David Araújo Tostes, Camila Povoa, Marinete Marins Quaresma, Juarez Antonio Simões Xavier, Marília Brasil Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region |
title | Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region |
title_full | Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region |
title_fullStr | Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region |
title_full_unstemmed | Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region |
title_short | Prevalence of autoantibodies against cellular antigens in patients with HIV and leprosy coinfection in the Amazon region |
title_sort | prevalence of autoantibodies against cellular antigens in patients with hiv and leprosy coinfection in the amazon region |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452639/ https://www.ncbi.nlm.nih.gov/pubmed/28566085 http://dx.doi.org/10.1186/s40249-017-0294-2 |
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