ALBERTO JOSE DA SILVA DUARTE

(Fonte: Lattes)
Índice h a partir de 2011
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Lattes
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Departamento de Patologia, Faculdade de Medicina - Docente
LIM/56 - Laboratório de Investigação em Dermatologia e Imunodeficiências, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/03 - Laboratório de Medicina Laboratorial, Hospital das Clínicas, Faculdade de Medicina

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  • article 14 Citação(ões) na Scopus
    Mucosal and systemic anti-GAG immunity induced by neonatal immunization with HIV LAMP/gag DNA vaccine in mice
    (2011) GOLDONI, Adriana Leticia; MACIEL JR., Milton; RIGATO, Paula Ordonhez; PIUBELLI, Orlando; BRITO, Cyro Alves de; MELO, Andrea; MARQUES, Ernesto Torres; AUGUST, Joseph Thomas; DUARTE, Alberto Jose da Silva; SATO, Maria Notomi
    Vaccines capable of inducing mucosal immunity in early postnatal life until adulthood, protecting early sexual initiation, should be considered as strategies to vaccination against HIV. The HIV-1 GAG protein as a chimera with the lysosome-associated membrane protein (LAMP/gag), encoded by a DNA vaccine, is targeted to the endosomal/lysosomal compartment that contains class II MHC molecules and has been shown to be immunogenic in adult mice. Assuming that one such strategy could help to overcome the immunological immaturity in the early postnatal period, we have evaluated the systemic and mucosal immunogenicity of LAMP/gag immunization in neonatal mice. Intranasal immunization with LAMP/gag vaccine induced higher levels of sIgA and IgG anti-GAG antibodies in intestinal washes than did the gag vaccine. The combination of ID injections and the IN protocol with the chimeric vaccine promoted the increase of Ab levels in sera. Both vaccines induced splenic IFN-gamma- secreting cells against GAG peptide pools, as well as in vivo cytotoxic T lymphocyte (CTL) function, and increased the percentage of CD8+ T cells to the immunodominant class I peptide in gut and spleen. However, only the chimeric vaccine was able to enhance Th1/Th2 cytokine secretion in response to class II GAG peptide and to enhance IL-4-secreting cells against GAG peptides and p24 protein stimuli. Long-lasting humoral and cellular responses were detected until adult age, following neonatal immunization with the chimeric vaccine. The LAMP/gag vaccination was able to induce potent GAG-specific T and B cell immune responses in early life which are essential to elicit sustained and long-lasting mucosal and systemic humoral response.
  • article 21 Citação(ões) na Scopus
    Impaired IFN-alpha secretion by plasmacytoid dendritic cells induced by TLR9 activation in chronic idiopathic urticaria
    (2011) FUTATA, E.; AZOR, M.; SANTOS, J. Dos; MARUTA, C.; SOTTO, M.; GUEDES, F.; RIVITTI, E.; DUARTE, A.; SATO, M.
    P>Background The evolution and therapeutic outcome of American tegumentary leishmaniasis (ATL) depend upon many factors, including the balance between Th1 and Th2 cytokines to control parasite multiplication and lesion extension. Other cytokines known for their role in inflammatory processes such as interleukin IL-17 or IL-18 as well as factors controlling keratinocyte differentiation and the inflammatory process in the skin, like the Notch system, could also be involved in the disease outcome. Notch receptors are a group of transmembrane proteins that regulate cell fate decisions during development and adulthood in many tissues, including keratinocyte differentiation and T-cell lineage commitment, depending on their activation by specific groups of ligands (Delta-like or Jagged). Objectives To compare the in situ expression of Notch system proteins (receptors, ligands and transcriptional factors) and cytokines possibly involved in the disease outcome (IL-17, IL-18, IL-23 and transforming growth factor-beta) in ATL cutaneous and mucosal lesions, according to the response to therapy with N-methyl glucamine. Methods Cutaneous and mucosal biopsies obtained from patients prior to therapy with N-methyl glucamine were analysed by immunohistochemistry and real-time polymerase chain reaction. Results Notch receptors and Delta-like ligands were found increased in patients with ATL, particularly those with poor response to therapy or with mucosal lesions. Conclusions The increase of Notch receptors and Delta-like ligands in patients with a poor response to treatment suggests that these patients would require a more aggressive therapeutic approach or at least a more thorough and rigorous follow-up.
  • article 26 Citação(ões) na Scopus
    Statin effects on regulatory and proinflammatory factors in chronic idiopathic urticaria
    (2011) AZOR, M. H.; SANTOS, J. C. dos; FUTATA, E. A.; BRITO, C. A. de; MARUTA, C. W.; RIVITTI, E. A.; DUARTE, A. J. da Silva; SATO, M. N.
    Immunological dysfunction has been described to occur in chronic idiopathic urticaria (CIU), most notably in association with an inflammatory process. Some pharmacological agents as statins - drugs used in hypercholesterolaemia - display a broad effect on the immune response and thus should be tested in vitro in CIU. Our main objectives were to evaluate the effects of statins on the innate and adaptive immune response in CIU. Simvastatin or lovastatin have markedly inhibited the peripheral blood mononuclear cells (PBMC) proliferative response induced by T and B cell mitogens, superantigen or recall antigen. Simvastatin arrested phytohaemaglutinin (PHA)induced T cells at the G0/G1 phase, inhibiting T helper type 1 (Th1), Th2, interleukin (IL)-10 and IL-17A cytokine secretion in both patients and healthy control groups. Up-regulation of suppressor of cytokine signalling 3 (SOCS3) mRNA expression in PHA-stimulated PBMCs from CIU patients was not modified by simvastatin, in contrast to the enhancing effect in the control group. Statin exhibited a less efficient inhibition effect on cytokine production [ IL-6 and macrophage inflammatory protein (MIP)-1 alpha] induced by Toll-like receptor (TLR)-4, to which a statin preincubation step was required. Furthermore, statin did not affect the tumour necrosis factor (TNF)-alpha secretion by lipopolysaccharide (LPS)-stimulated PBMC or CD14(+) cells in CIU patients. In addition, LPS-activated PBMC from CIU patients showed impaired indoleamine 2,3-dioxygenase (IDO) mRNA expression compared to healthy control, which remained at decreased levels with statin treatment. Statins exhibited a marked down-regulatory effect in T cell functions, but were not able to control TLR-4 activation in CIU patients. The unbalanced regulatory SOCS3 and IDO expressions in CIU may contribute to the pathogenesis of the disease.
  • article 12 Citação(ões) na Scopus
    Efeitos da radiação solar crônica prolongada sobre o sistema imunológico de pescadores profissionais em Recife (PE), Brasil
    (2011) BEZERRA, Sarita Maria de Fatima Martins de Carvalho; SOTTO, Mirian Nakagami; ORII, Noemia Mie; ALVES, Cleiton; DUARTE, Alberto Jose da Silva
    BACKGROUND: Among the various occupations which necessarily require long-term and chronic sun exposure is that of a fisherman. However, clinical experience in dermatology earned over several years of medical practice does not seem to confirm this hypothesis. OBJECTIVE: To evaluate clinical, histological and immunological effects of long-term and chronic exposure to ultraviolet radiation in fishermen. METHODS: A prospective, cross-sectional and observational study characterized skin lesions, immunological markers and histological alterations in fishermen, as well as lymphocyte subpopulations compared to a control group. Mann-Whitney, Fisher's and Wilcoxon statistical tests were used at a significance level of 0.05. RESULTS: There were significant differences between the exposed group and the group protected due to elastosis (p = 0.03), ectasia of dermal vessels (p = 0.012) and number of cells in the epidermal layers between cones (p = 0.029). Most common among fishermen were CD45RO, CD68 + and mastocytes in the skin (p = 0.040, p < 0.001, p = 0.001) and CD3CD8CD45RO in the blood (p = 0.016). CONCLUSION: The alterations suggest that long-term and chronic sun exposure promotes tolerance to ultraviolet radiation, which protects against immunosuppression.
  • article 506 Citação(ões) na Scopus
    IRF8 Mutations and Human Dendritic-Cell Immunodeficiency
    (2011) HAMBLETON, Sophie; SALEM, Sandra; BUSTAMANTE, Jacinta; BIGLEY, Venetia; BOISSON-DUPUIS, Stephanie; AZEVEDO, Joana; FORTIN, Anny; HANIFFA, Muzlifah; CERON-GUTIERREZ, Lourdes; BACON, Chris M.; MENON, Geetha; TROUILLET, Celine; MCDONALD, David; CAREY, Peter; GINHOUX, Florent; ALSINA, Laia; ZUMWALT, Timothy J.; KONG, Xiao-Fei; KUMARARATNE, Dinakantha; BUTLER, Karina; HUBEAU, Marjorie; FEINBERG, Jacqueline; AL-MUHSEN, Saleh; CANT, Andrew; ABEL, Laurent; CHAUSSABEL, Damien; DOFFINGER, Rainer; TALESNIK, Eduardo; GRUMACH, Anete; DUARTE, Alberto; ABARCA, Katia; MORAES-VASCONCELOS, Dewton; BURK, David; BERGHUIS, Albert; GEISSMANN, Frederic; COLLIN, Matthew; CASANOVA, Jean-Laurent; GROS, Philippe
    BACKGROUND The genetic analysis of human primary immunodeficiencies has defined the contribution of specific cell populations and molecular pathways in the host defense against infection. Disseminated infection caused by bacille Calmette-Guerin (BCG) vaccines is an early manifestation of primary immunodeficiencies, such as severe combined immunodeficiency. In many affected persons, the cause of disseminated BCG disease is unexplained. METHODS We evaluated an infant presenting with features of severe immunodeficiency, including early-onset disseminated BCG disease, who required hematopoietic stem-cell transplantation. We also studied two otherwise healthy subjects with a history of disseminated but curable BCG disease in childhood. We characterized the monocyte and dendritic-cell compartments in these three subjects and sequenced candidate genes in which mutations could plausibly confer susceptibility to BCG disease. RESULTS We detected two distinct disease-causing mutations affecting interferon regulatory factor 8 (IRF8). Both K108E and T80A mutations impair IRF8 transcriptional activity by disrupting the interaction between IRF8 and DNA. The K108E variant was associated with an autosomal recessive severe immunodeficiency with a complete lack of circulating monocytes and dendritic cells. The T80A variant was associated with an autosomal dominant, milder immunodeficiency and a selective depletion of CD11c+CD1c+ circulating dendritic cells. CONCLUSIONS These findings define a class of human primary immunodeficiencies that affect the differentiation of mononuclear phagocytes. They also show that human IRF8 is critical for the development of monocytes and dendritic cells and for antimycobacterial immunity. (Funded by the Medical Research Council and others.)
  • article 74 Citação(ões) na Scopus
    Reduced seroprotection after pandemic H1N1 influenza adjuvant-free vaccination in patients with rheumatoid arthritis: implications for clinical practice
    (2011) RIBEIRO, Ana C. M.; GUEDES, Lissiane K. N.; MORAES, Julio C. B.; SAAD, Carla G. S.; AIKAWA, Nadia E.; CALICH, Ana Luisa; FRANCA, Ivan L. A.; CARVALHO, Jozelio F.; SAMPAIO-BARROS, Percival D.; GONCALVES, Celio R.; BORBA, Eduardo F.; TIMENETSKY, Maria do Carmo S.; PRECIOSO, Alexander R.; DUARTE, Alberto; BONFA, Eloisa; LAURINDO, Ieda M. M.
    Background Reduced response to pandemic (2009) H1N1 (pH1N1) vaccine in patients with rheumatoid arthritis (RA) was recently reported. Objectives To evaluate the contribution of age, disease activity, medication and previous antibody levels to this reduced response. Methods 340 adult RA patients and 234 healthy controls were assessed before and 21 days after adjuvant-free influenza A/California/7/2009 (pH1N1) vaccine. Disease activity (DAS28), current treatment and pH1N1 antibody titres were collected. Seroprotection, seroconversion and factor increase in geometric mean titre (GMT) were calculated and adverse events registered. Results RA and controls showed similar (p> 0.05) prevaccination GMT (8.0 vs 9.3) and seroprotection (10.8% vs 11.5%). After vaccination a significant reduction (p< 0.001) was observed in all endpoints: GMT and factor increase in GMT, seroprotection and seroconversion rates. Disease activity did not preclude seroconversion or seroprotection and remained unchanged in 97.4% of patients. Methotrexate was the only disease-modifying antirheumatic drug associated with reduced responses (p= 0.001). Vaccination was well tolerated. Conclusions The data confirmed both short-term anti-pH1N1 vaccine safety and, different from most studies with seasonal influenza, reduced seroprotection in RA patients, unrelated to disease activity and to most medications (except methotrexate). Extrapolation of immune responses from one vaccine to another may therefore not be possible and specific immunisation strategies (possibly booster) may be needed.