Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients
Autor(a) principal: | |
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Data de Publicação: | 2012 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/34728 http://dx.doi.org/10.1111/j.1365-2249.2011.04538.x |
Resumo: | Several studies correlated genetic background and pancreatic islet-cell autoantibody status (type and number) in type 1A diabetes mellitus (T1AD), but there are no data evaluating the relationship among these markers with serum cytokines, regulatory T cells and beta cell function. This characterization has a potential importance with regard to T1AD patients' stratification and follow-up in therapeutic prevention. in this study we showed that peripheral sera cytokines [interleukin (IL)-12, IL-6, II-1 beta, tumour necrosis factor (TNF)-a, IL-10] and chemokines (CXCL10, CXCL8, CXCL9, CCL2) measured were significantly higher in newly diagnosed T1AD patients when compared to healthy controls (P < 0.001). Among T1AD, we found a positive correlation between CXCL10 and CCL-2 (r = 0.80; P = 0.000), IL-8 and TNF-alpha (r = 0.60; P = 0.000); IL-8 and IL-12 (r = 0.57; P = 0.001) and TNF-alpha and IL-12 (r = 0.93; P = 0.000). Glutamic acid decarboxylase-65 (GAD-65) autoantibodies (GADA) were associated negatively with CXCL10 (r = -0.45; P = 0.011) and CCL2 (r = -0.65; P = 0.000), while IA-2A showed a negative correlation with IL-10 (r = -0.38; P = 0.027). Human leucocyte antigen (HLA) DR3, DR4 or DR3/DR4 and PTPN22 polymorphism did not show any association with pancreatic islet cell antibodies or cytokines studied. in summary, our results revealed that T1AD have a proinflammatory cytokine profile compared to healthy controls and that IA-2A sera titres seem to be associated with a more inflammatory peripheral cytokine/chemokine profile than GADA. A confirmation of these data in the pre-T1AD phase could help to explain the mechanistic of the well-known role of IA-2A as a more specific marker of beta-cell damage than GADA during the natural history of T1AD. |
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Gabbay, Monica Andrade Lima [UNIFESP]Sato, M. N.Duarte, A. J. S.Dib, Sergio Atala [UNIFESP]Universidade Federal de São Paulo (UNIFESP)São Paulo State Univ2016-01-24T14:27:00Z2016-01-24T14:27:00Z2012-04-01Clinical and Experimental Immunology. Malden: Wiley-Blackwell, v. 168, n. 1, p. 60-67, 2012.0009-9104http://repositorio.unifesp.br/handle/11600/34728http://dx.doi.org/10.1111/j.1365-2249.2011.04538.x10.1111/j.1365-2249.2011.04538.xWOS:000300974800010Several studies correlated genetic background and pancreatic islet-cell autoantibody status (type and number) in type 1A diabetes mellitus (T1AD), but there are no data evaluating the relationship among these markers with serum cytokines, regulatory T cells and beta cell function. This characterization has a potential importance with regard to T1AD patients' stratification and follow-up in therapeutic prevention. in this study we showed that peripheral sera cytokines [interleukin (IL)-12, IL-6, II-1 beta, tumour necrosis factor (TNF)-a, IL-10] and chemokines (CXCL10, CXCL8, CXCL9, CCL2) measured were significantly higher in newly diagnosed T1AD patients when compared to healthy controls (P < 0.001). Among T1AD, we found a positive correlation between CXCL10 and CCL-2 (r = 0.80; P = 0.000), IL-8 and TNF-alpha (r = 0.60; P = 0.000); IL-8 and IL-12 (r = 0.57; P = 0.001) and TNF-alpha and IL-12 (r = 0.93; P = 0.000). Glutamic acid decarboxylase-65 (GAD-65) autoantibodies (GADA) were associated negatively with CXCL10 (r = -0.45; P = 0.011) and CCL2 (r = -0.65; P = 0.000), while IA-2A showed a negative correlation with IL-10 (r = -0.38; P = 0.027). Human leucocyte antigen (HLA) DR3, DR4 or DR3/DR4 and PTPN22 polymorphism did not show any association with pancreatic islet cell antibodies or cytokines studied. in summary, our results revealed that T1AD have a proinflammatory cytokine profile compared to healthy controls and that IA-2A sera titres seem to be associated with a more inflammatory peripheral cytokine/chemokine profile than GADA. A confirmation of these data in the pre-T1AD phase could help to explain the mechanistic of the well-known role of IA-2A as a more specific marker of beta-cell damage than GADA during the natural history of T1AD.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Federal de São Paulo, Ctr Diabet, Div Endocrinol, Dept Med, BR-04039032 São Paulo, BrazilSão Paulo State Univ, Immunol Lab, São Paulo, BrazilUniversidade Federal de São Paulo, Ctr Diabet, Div Endocrinol, Dept Med, BR-04039032 São Paulo, BrazilWeb of Science60-67engWiley-BlackwellClinical and Experimental Immunologyhttp://olabout.wiley.com/WileyCDA/Section/id-406071.htmlinfo:eu-repo/semantics/openAccesscytokinepancreatic autoantibodiesregulatory T cellstype 1 diabetesSerum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patientsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/347282023-02-15 09:30:31.14metadata only accessoai:repositorio.unifesp.br:11600/34728Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-02-15T12:30:31Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients |
title |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients |
spellingShingle |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients Gabbay, Monica Andrade Lima [UNIFESP] cytokine pancreatic autoantibodies regulatory T cells type 1 diabetes |
title_short |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients |
title_full |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients |
title_fullStr |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients |
title_full_unstemmed |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients |
title_sort |
Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients |
author |
Gabbay, Monica Andrade Lima [UNIFESP] |
author_facet |
Gabbay, Monica Andrade Lima [UNIFESP] Sato, M. N. Duarte, A. J. S. Dib, Sergio Atala [UNIFESP] |
author_role |
author |
author2 |
Sato, M. N. Duarte, A. J. S. Dib, Sergio Atala [UNIFESP] |
author2_role |
author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) São Paulo State Univ |
dc.contributor.author.fl_str_mv |
Gabbay, Monica Andrade Lima [UNIFESP] Sato, M. N. Duarte, A. J. S. Dib, Sergio Atala [UNIFESP] |
dc.subject.eng.fl_str_mv |
cytokine pancreatic autoantibodies regulatory T cells type 1 diabetes |
topic |
cytokine pancreatic autoantibodies regulatory T cells type 1 diabetes |
description |
Several studies correlated genetic background and pancreatic islet-cell autoantibody status (type and number) in type 1A diabetes mellitus (T1AD), but there are no data evaluating the relationship among these markers with serum cytokines, regulatory T cells and beta cell function. This characterization has a potential importance with regard to T1AD patients' stratification and follow-up in therapeutic prevention. in this study we showed that peripheral sera cytokines [interleukin (IL)-12, IL-6, II-1 beta, tumour necrosis factor (TNF)-a, IL-10] and chemokines (CXCL10, CXCL8, CXCL9, CCL2) measured were significantly higher in newly diagnosed T1AD patients when compared to healthy controls (P < 0.001). Among T1AD, we found a positive correlation between CXCL10 and CCL-2 (r = 0.80; P = 0.000), IL-8 and TNF-alpha (r = 0.60; P = 0.000); IL-8 and IL-12 (r = 0.57; P = 0.001) and TNF-alpha and IL-12 (r = 0.93; P = 0.000). Glutamic acid decarboxylase-65 (GAD-65) autoantibodies (GADA) were associated negatively with CXCL10 (r = -0.45; P = 0.011) and CCL2 (r = -0.65; P = 0.000), while IA-2A showed a negative correlation with IL-10 (r = -0.38; P = 0.027). Human leucocyte antigen (HLA) DR3, DR4 or DR3/DR4 and PTPN22 polymorphism did not show any association with pancreatic islet cell antibodies or cytokines studied. in summary, our results revealed that T1AD have a proinflammatory cytokine profile compared to healthy controls and that IA-2A sera titres seem to be associated with a more inflammatory peripheral cytokine/chemokine profile than GADA. A confirmation of these data in the pre-T1AD phase could help to explain the mechanistic of the well-known role of IA-2A as a more specific marker of beta-cell damage than GADA during the natural history of T1AD. |
publishDate |
2012 |
dc.date.issued.fl_str_mv |
2012-04-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:27:00Z |
dc.date.available.fl_str_mv |
2016-01-24T14:27:00Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Clinical and Experimental Immunology. Malden: Wiley-Blackwell, v. 168, n. 1, p. 60-67, 2012. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/34728 http://dx.doi.org/10.1111/j.1365-2249.2011.04538.x |
dc.identifier.issn.none.fl_str_mv |
0009-9104 |
dc.identifier.doi.none.fl_str_mv |
10.1111/j.1365-2249.2011.04538.x |
dc.identifier.wos.none.fl_str_mv |
WOS:000300974800010 |
identifier_str_mv |
Clinical and Experimental Immunology. Malden: Wiley-Blackwell, v. 168, n. 1, p. 60-67, 2012. 0009-9104 10.1111/j.1365-2249.2011.04538.x WOS:000300974800010 |
url |
http://repositorio.unifesp.br/handle/11600/34728 http://dx.doi.org/10.1111/j.1365-2249.2011.04538.x |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Clinical and Experimental Immunology |
dc.rights.driver.fl_str_mv |
http://olabout.wiley.com/WileyCDA/Section/id-406071.html info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
http://olabout.wiley.com/WileyCDA/Section/id-406071.html |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
60-67 |
dc.publisher.none.fl_str_mv |
Wiley-Blackwell |
publisher.none.fl_str_mv |
Wiley-Blackwell |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
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1802764192472629248 |