DEWTON DE MORAES VASCONCELOS

(Fonte: Lattes)
Índice h a partir de 2011
11
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/56 - Laboratório de Investigação em Dermatologia e Imunodeficiências, Hospital das Clínicas, Faculdade de Medicina
LIM/31 - Laboratório de Genética e Hematologia Molecular, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 6 de 6
  • conferenceObject
    PARACOCCIDIOIDOMYCOSIS AS A NEW (AND AWAITED) INFECTIOUS DISEASE IN GATA2 DEFICIENCY
    (2016) MORAES-VASCONCELOS, Dewton; MOREIRA, Nathalia; RUIZ, Antonio Lancha; NARDINELLI, Luciana; BARROS, Noac Chuffi; KHOURY, Zarifa; BENDIT, Israel
  • article 8 Citação(ões) na Scopus
    Chemokine, cytokine and type I interferon production induced by Toll-like receptor activation in common variable immune deficiency
    (2016) LOLLO, Camila de; VASCONCELOS, Dewton de Moraes; OLIVEIRA, Luanda Mara da Silva; DOMINGUES, Rosana; CARVALHO, Gabriel Costa de; DUARTE, Alberto Jose da Silva; SATO, Maria Notomi
    Common variable immunodeficiency (CVID) is the most common symptomatic primary antibody deficiency and is associated with recurrent infections and chronic inflammatory diseases. We evaluated the ability of Toll-like receptor (TLR) ligands to induce secretion of chemokines, cytokines and type I interferons by peripheral blood mononuclear cells (PBMCs) from CVID patients. High levels of CXCL10, CCL2, CXCL9, CCL5, CXCL8, and IL-6 were detected in sera of CVID patients compared with healthy controls. Increased chemokine levels were observed in unstimulated PBMCs, but after stimulation with TLR2 and TLR4 agonists, equivalent chemokine and pro-inflammatory cytokine secretion, as in healthy controls, was observed, whereas TLR4 agonist induced a decreased secretion of CCL2 and CXCL8 and increased secretion of TNF. Decreased IFN-alpha secretion induced by TLR7/TLR8 activation was observed in CVID, which was recovered with TLR9 signaling. Our findings revealed that TLR9 activation has an adjuvant effect on the altered type I response in CVID.
  • article 12 Citação(ões) na Scopus
    Disseminated cryptococcosis manifested as a single tumor in an immunocompetent patient, similar to the cutaneous primary forms
    (2016) AMARAL, Danielle Mechereffe do; CARNEIRO, Luiz Euribel Prestes; ABREU, Marilda Aparecida Milanez Morgado de; ROCHA, Ritha de Cassia Capelato; VASCONCELOS, Dewton Moraes
    Cryptococcosis is a fungal infection caused by Cryptococcus neoformans that tends to affect immunocompromised individuals. The fungi are mostly acquired by inhalation, which leads to an initial pulmonary infection. Later, other organs-such as the central nervous system and the skin - can be affected by hematogenous spread. In addition, cutaneous contamination can occur by primary inoculation after injuries (primary cutaneous cryptococcosis), whose diagnosis is defined based on the absence of systemic involvement. The clinical presentation of cutaneous forms typically vary according to the infection mode. We report an unusual case of disseminated cryptococcosis in an immunocompetent patient with cutaneous lesions similar to those caused by primary inoculation. This clinical picture leads us to question the definition of primary cutaneous cryptococcosis established in the literature.
  • conferenceObject
    APECED AUTOIMMUNE POLYENDOCRINOPATHY WITH CANDIDIASIS AND ECTODERMAL DYSTROPHY AND ESOPHAGEAL RUPTURE BY CANDIDIASIS IMMUNODEFICIENCY
    (2016) BERTOLINI, Dalton Luis; MORAES-VASCONCELOS, Dewton; DOMINGUES-FERREIRA, Mauricio; BEZERRA, Thiago de Almeida
  • conferenceObject
    MCM4 DEFICIENCY: A RARE VARIANT OF IMMUNODEFICIENCY OF NK CELLS ASSOCIATED TO PROPORTIONATE NANISM AND ADRENAL INSUFFICIENCY. DESCRIPTION OF THE FIRST CASE IN BRAZIL
    (2016) MORAES-VASCONCELOS, Dewton; RIBEIRO, Roberto; RIGATO, Paula Ordonhez; PINICHI, Paula; AOKI, Valeria; TAKAOKA, Roberto; DUARTE, Alberto Jose da Silva; SABINO, Ester Cerdeira
  • article 14 Citação(ões) na Scopus
    Impaired CD8(+) T cell responses upon Toll-like receptor activation in common variable immunodeficiency
    (2016) LOLLO, Camila de; VASCONCELOS, Dewton de Moraes; OLIVEIRA, Luanda Mara da Silva; TITZ, Tiago de Oliveira; CARNEIRO-SAMPAIO, Magda; JACOB, Cristina Miuki Abe; DUARTE, Alberto Jose da Silva; SATO, Maria Notomi
    Background: Infections caused by bacteria or viruses are frequent in common variable immunodeficiency (CVID) patients due to antibody deficiencies, which may be associated with altered T cell function. CVID patients are frequently in contact with pathogen-associated molecular patterns (PAMPs), leading to the activation of innate immunity through Toll-like receptors (TLR) affecting T cell activation. We evaluated the effect of TLR activation on T cells in CVID patients undergoing intravenous immunoglobulin (IVIg) replacement using synthetic ligands. Methods: Expression of exhaustion, activation and maturation markers on T cells from peripheral blood as well as regulatory T cells and follicular T cells in peripheral blood mononuclear cells (PBMCs) from CVID and healthy individuals were evaluated by flow cytometry. PBMCs cultured with TLR agonists were assessed for intracellular IFN-gamma, TNF, IL-10, IL-17a or IL-22 secretion as monofunctional or polyfunctional T cells (simultaneous cytokine secretion) by flow cytometry. Results: We found increased expression of the exhaustion marker PD-1 on effector memory CD4(+) T cells (CD45RA(-)CCR7(-)) in the peripheral blood and increased expression of CD38 in terminally differentiated CD8(+) T cells (CD45RA(+)CCR7(-)). Furthermore, a decreased frequency of naive regulatory T cells (CD45RA(+)Foxp3(low)), but not of activated regulatory T cells (CD45RA(-)Foxp3(high)) was detected in CVID patients with splenomegaly, the noninfectious manifestation in this CVID cohort (43.7 %). Moreover, the frequency of peripheral blood follicular helper T cells (CD3(+)CD4(+)CXCR5(+)PD-1(+)ICOS(+)) was similar between the CVID and control groups. Upon in vitro TLR3 activation, a decreased frequency of CD8(+) T cells secreting IFN-gamma, IL-17a or IL-22 was detected in the CVID group compared to the control group. However, a TLR7/TLR8 agonist and staphylococcal enterotoxin B induced an increased Th22/Tc22 (IL-22(+), IFN-gamma(-), IL-17a(-)) response in CVID patients. Both TLR2 and TLR7/8/CL097 activation induced an increased response of CD4(+) T cells secreting three cytokines (IL-17a, IL-22 and TNF) in CVID patients, whereas CD8(+) T cells were unresponsive to these stimuli. Conclusion: The data show that despite the unresponsive profile of CD8(+) T cells to TLR activation, CD4(+) T cells and Tc22/Th22 cells are responsive, suggesting that activation of innate immunity by TLRs could be a strategy to stimulate CD4(+) T cells in CVID.