MARIA NOTOMI SATO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Dermatologia, Faculdade de Medicina - Docente
LIM/56 - Laboratório de Investigação em Dermatologia e Imunodeficiências, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/56 - Laboratório de Investigação em Dermatologia e Imunodeficiências, Hospital das Clínicas, Faculdade de Medicina - Líder
5 resultados
Resultados de Busca
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- 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.
- The dysfunctional innate immune response triggered by Toll-like receptor activation is restored by TLR7/TLR8 and TLR9 ligands in cutaneous lichen planus(2015) DOMINGUES, R.; CARVALHO, G. Costa de; OLIVEIRA, L. M. da Silva; TANIGUCHI, E. Futata; ZIMBRES, J. M.; AOKI, V.; DUARTE, A. J. da Silva; SATO, M. N.BackgroundLichen planus (LP) is a chronic inflammatory mucocutaneous disease. Toll-like receptors (TLRs) bind numerous exogenous and endogenous antigens by recognizing conserved pathogen-associated molecular patterns (PAMPs) and have the ability to induce the production of proinflammatory cytokines. Therefore, alterations in innate immunity could explain the inflammation and T-cell autoreactivity leading to the development of LP disease. ObjectivesTo evaluate how the host innate immune response to PAMPs is affected by cutaneous LP, primarily by using TLR agonists to induce proinflammatory cytokine secretion from peripheral blood mononuclear cells (PBMCs). MethodsPBMCs from patients with LP and healthy control (HC) individuals were stimulated with agonists of TLR2/TLR1 (pam3csk4), TLR3 [poly(I:C)-RIG], TLR4 (lipopolysaccharide), TLR5 (flagellin), TLR7 (imiquimod), TLR7/TLR8 (CL097) and TLR9 (CpG). Cytokines from culture supernatants (n=10-12) andserum chemokines and cytokines (n=22-24) were measured using flow cytometry. ResultsActivation through the TLR2, TLR4 and TLR5 pathways induced increased tumour necrosis factor (TNF)- secretion by PBMCs from individuals with LP compared with the HC group. In contrast, activation through TLR3 and TLR7 was impaired in the LP group, leading to decreased TNF- secretion. Moreover, intracellular TLR activation resulted in reduced interleukin (IL)-1 and IL-6 secretion. Notably, individuals with LP became responders on stimulation with TLR7/TLR8 and TLR9 agonists; responses were measured as increases in interferon (IFN)- production. Detectable TNF- and high CXCL9 and CXCL10 serum levels were observed in patients with LP, suggesting their potential use as markers of the inflammatory status in LP. ConclusionsThese findings point to a defect in the TLR signalling pathways in cutaneous LP. Agonists of TLR7/TLR8 or TLR9 overcame impaired IFN- secretion in LP, strategically acting as adjuvants to improve the type I response.
conferenceObject Phenotypic profile of CLA plus natural killer cells in adults with atopic dermatitis(2018) ORFALI, R. L.; LIMA, J. F.; CARVALHO, G. C. C.; RAMOS, Y. A. L.; DUARTE, A. J. S.; SATO, M.; AOKI, V.conferenceObject Eosinophilia in patients with atopic dermatitis is associated with increased expression of CCR3 and decreased expression of CD23 and CD62L(2014) TITZI, T. D. O.; SANTOS, V. G. D.; LOLLO, C. D.; ORFALI, R. L.; DUARTE, A. J. D. S.; SATO, M. N.; AOKI, V.conferenceObject Evaluation of polyfunctional T cells to staphylococcal enterotoxins A and B in adults with atopic dermatitis(2014) ORFALI, R. L.; SATO, M. N.; OLIVEIRA, L. M. S.; SANTOS, V. G. D.; TITZ, T. D. O.; LOLLO, C. de; AOKI, V.