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DC Field | Value | Language |
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dc.contributor | Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP | - |
dc.contributor.author | GABBAY, M. Andrade Lima | - |
dc.contributor.author | SATO, M. N. | - |
dc.contributor.author | DUARTE, A. J. S. | - |
dc.contributor.author | DIB, S. A. | - |
dc.date.accessioned | 2014-01-28T22:20:32Z | - |
dc.date.available | 2014-01-28T22:20:32Z | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | CLINICAL AND EXPERIMENTAL IMMUNOLOGY, v.168, n.1, p.60-67, 2012 | - |
dc.identifier.issn | 0009-9104 | - |
dc.identifier.uri | https://observatorio.fm.usp.br/handle/OPI/4037 | - |
dc.description.abstract | 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. | - |
dc.description.sponsorship | FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) | - |
dc.description.sponsorship | CAPES-PROEX (Coordenadoria de Aperfeicoamento do Pessoal de Ensino Superior-Programas de Excelencia)- Ministry of Education of Brazil | - |
dc.language.iso | eng | - |
dc.publisher | WILEY-BLACKWELL | - |
dc.relation.ispartof | Clinical and Experimental Immunology | - |
dc.rights | restrictedAccess | - |
dc.subject | cytokine | - |
dc.subject | pancreatic autoantibodies | - |
dc.subject | regulatory T cells | - |
dc.subject | type 1 diabetes | - |
dc.subject.other | beta-cell function | - |
dc.subject.other | hla-class-ii | - |
dc.subject.other | autoimmune-diseases | - |
dc.subject.other | natural-history | - |
dc.subject.other | c-peptide | - |
dc.subject.other | cytokines | - |
dc.subject.other | children | - |
dc.subject.other | mellitus | - |
dc.subject.other | ptpn22 | - |
dc.subject.other | onset | - |
dc.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 | - |
dc.type | article | - |
dc.rights.holder | Copyright WILEY-BLACKWELL | - |
dc.identifier.doi | 10.1111/j.1365-2249.2011.04538.x | - |
dc.identifier.pmid | 22385239 | - |
dc.subject.wos | Immunology | - |
dc.type.category | original article | - |
dc.type.version | publishedVersion | - |
hcfmusp.author.external | GABBAY, M. Andrade Lima:Univ Fed Sao Paulo, Ctr Diabet, Div Endocrinol, Dept Med, BR-04039032 Sao Paulo, Brazil | - |
hcfmusp.author.external | DIB, S. A.:Univ Fed Sao Paulo, Ctr Diabet, Div Endocrinol, Dept Med, BR-04039032 Sao Paulo, Brazil | - |
hcfmusp.description.beginpage | 60 | - |
hcfmusp.description.endpage | 67 | - |
hcfmusp.description.issue | 1 | - |
hcfmusp.description.volume | 168 | - |
hcfmusp.origem | WOS | - |
hcfmusp.origem.id | 2-s2.0-84857700615 | - |
hcfmusp.origem.id | WOS:000300974800010 | - |
hcfmusp.publisher.city | MALDEN | - |
hcfmusp.publisher.country | USA | - |
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dc.description.index | MEDLINE | - |
hcfmusp.remissive.sponsorship | CAPES | - |
hcfmusp.remissive.sponsorship | FAPESP | - |
hcfmusp.lim.ref | 2012 | - |
hcfmusp.citation.scopus | 30 | - |
hcfmusp.scopus.lastupdate | 2024-04-12 | - |
Appears in Collections: | Artigos e Materiais de Revistas Científicas - FM/MDT Artigos e Materiais de Revistas Científicas - FM/MPT Artigos e Materiais de Revistas Científicas - HC/ICHC Artigos e Materiais de Revistas Científicas - LIM/03 Artigos e Materiais de Revistas Científicas - LIM/56 |
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