JORGE ELIAS KALIL FILHO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina - Docente
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/19 - Laboratório de Histocompatibilidade e Imunidade Celular, Hospital das Clínicas, Faculdade de Medicina - Líder
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/19 - Laboratório de Histocompatibilidade e Imunidade Celular, Hospital das Clínicas, Faculdade de Medicina - Líder
31 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 31
conferenceObject Esophagogastroduodenal Mucosal Behavior after Bronchial Challenge with House Dust Mites in Allergic Asthmatic Patients(2015) AGONDI, Rosana C.; NAVARRO-RODRIGUEZ, Tomas; BARBUTI, Ricardo; BISACCIONI, Carla; AUN, Marcelo Vivolo; KALIL, Jorge; GIAVINA-BIANCHI, PedroconferenceObject Bordetella Pertussis Whole-Cell Vaccine Inhibits Specific IgE, Inflammation and Airway Remodeling in a Murine Model of Asthma(2015) AUN, Marcelo Vivolo; ARANTES-COSTA, Fernanda; SARAIVA-ROMANHOLO, Beatriz Mangueira; ALMEIDA, Francine Maria; REGINA-BRUEGGERMANN, Thayse; MARTINS, Milton Arruda; KALIL, Jorge; GIAVINA-BIANCHI, Pedro- The Absence of CYP3A5*3 Is a Protective Factor to Anticonvulsants Hypersensitivity Reactions: A Case-Control Study in Brazilian Subjects (vol 10, e0136141, 2015)(2015) TANNO, Luciana Kase; KERR, Daniel Shikanai; SANTOS, Bernardo dos; TALIB, Leda Leme; YAMAGUTI, Celia; RODRIGUES, Helcio; GATTAZ, Wagner Farid; KALIL, Jorge
conferenceObject Altered Expression of BAFF-R and TACI in Common Variable Immunodeficiency (CVID) Patients(2015) SILVA, Diana Cordeiro de Oliveira; BARSOTTI, Nathalia Silveira; OLIVEIRA, Ana Karolina Barreto de; ZILINSKI, Fernando Ramon; BARROS, Myrthes Toledo; KALIL, Jorge; KOKRON, Cristina Maria- Rheumatic Fever: How Streptococcal Throat Infection Triggers an Autoimmune Disease(2015) GUILHERME, L.; KALIL, J.Molecular mimicry between streptococcal and human proteins has been proposed as the triggering factor leading to autoimmunity in rheumatic fever (RF) and rheumatic heart disease (RHD). Punctual genetic polymorphisms related to both innate and adaptive immune responses are involved in the development of RF/RHD. Some adhesion molecules and chemokines facilitate the monocytes and macrophages and T and B cell infiltration to the heart-tissue. Here we presented data on molecular mimicry mediated by B and T cell responses of peripheral blood and T cell clones infiltrating heart lesions from RHD patients against streptococcal antigens and human tissue proteins. The molecular analysis of T cell recognition is assessed by the definition of heart-cross reactive antigens. Degenerate patterns of T cell receptor (TCR) recognition in which intralesional T cell clones presenting the same TCR-BVJB and AVJB and recognized different antigens are described. The production of inflammatory cytokines such as TNFa, IL-2, IL-17, IL-23 and IFNg from peripheral and heart-infiltrating mononuclear cells, suggested that Th-1 and Th-17 type cytokines are the mediators of RHD heart lesions. All the results presented here delineate the mechanisms involved in RF/RHD and can certainly be a model for other autoimmune diseases. © 2015 Elsevier B.V. All rights reserved.
bookPart Imunizações(2015) KALIL, Jorge; MARINHO, Ana Karolina Barreto Berselli- Multiple Approaches for Increasing the Immunogenicity of an Epitope-Based Anti-HIV Vaccine(2015) ROSA, Daniela Santoro; RIBEIRO, Susan Pereira; FONSECA, Simone Goncalves; ALMEIDA, Rafael Ribeiro; SANTANA, Vinicius Canato; APOSTOLICO, Juliana de Souza; KALIL, Jorge; CUNHA-NETO, EdecioThe development of a highly effective vaccine against the human immunodeficiency virus (HIV) will likely be based on rational vaccine design, since traditional vaccine approaches have failed so far. In recent years, an understanding of what type of immune response is protective against infection and/or disease facilitated vaccine design. T cell-based vaccines against HIV have the goal of limiting both transmission and disease progression by inducing broad and functionally relevant T cell responses. In this context, CD4(+) T cells play a direct cytotoxic role and are also important for the generation and maintenance of functional CD8(+) T and B cell responses. The use of MHC-binding algorithms has allowed the identification of novel CD4(+) T cell epitopes that could be used in vaccine design, the so-called epitope-driven vaccine design. Epitope-based vaccines have the ability to focus the immune response on highly antigenic, conserved epitopes that are fully recognized by the target population. We have recently mapped a set of conserved multiple HLA-DR-binding HIV-1 CD4 epitopes and observed interferon (IFN)--producing CD4(+) T cells when we tested these peptides in peripheral blood mononuclear cells (PBMCs) from HIV-infected individuals. We then designed multiepitopic DNA vaccines that induced broad and polyfunctional T cell responses in immunized mice. In this review we will focus on alternative strategies to increase the immunogenicity of an epitope-based vaccine against HIV infection.
bookPart Terapêutica Monoclonal nas Doenças Alérgicas(2015) AGONDI, Rosana Câmara; GIAVINA-BIANCHI, Pedro; KALIL, Jorge- Functional IL18 polymorphism and susceptibility to Chronic Chagas Disease(2015) NOGUEIRA, Luciana Gabriel; FRADE, Amanda Farage; IANNI, Barbara Maria; LAUGIER, Laurie; PISSETTI, Cristina Wide; CABANTOUS, Sandrine; BARON, Monique; PEIXOTO, Gisele de Lima; BORGES, Ariana de Melo; DONADI, Eduardo; MARIN-NETO, Jose A.; SCHMIDT, Andre; DIAS, Fabricio; SABA, Bruno; WANG, Hui-Tzu Lin; FRAGATA, Abilio; SAMPAIO, Marcelo; HIRATA, Mario Hiroyuki; BUCK, Paula; MADY, Charles; MARTINELLI, Martino; LENSI, Mariana; SIQUEIRA, Sergio Freitas; PEREIRA, Alexandre Costa; RODRIGUES JR., Virmondes; KALIL, Jorge; CHEVILLARD, Christophe; CUNHA-NETO, EdecioBackground: Chronic Chagas Disease cardiomyopathy (CCC), a life-threatening inflammatory dilated cardiomyopathy, affects 30% of the approximately 8 million patients infected by Trypanosoma cruzi, the rest of the infected subjects remaining asymptomatic (ASY). The Th1 T cell-rich myocarditis plays a pivotal role in CCC pathogenesis. Local expression of IL-18 in CCC myocardial tissue has recently been described. IL-18 could potentially amplify the process by inducing increased expression of IFN-gamma which in turn can increase the production of IL-18, thereby creating a positive feedback mechanism. In order to assess the contribution of the IL-18 to susceptibility to Chronic Chagas Disease, we investigated the association between a single nucleotide polymorphism (SNP) located in the IL-18 gene with the risk of developing Chagas cardiomyopathy. Methods and results: We analyzed the rs2043055 marker in the 118 gene in a cohort of Chagas disease cardiomyopathy patients (n = 849) and asymptomatic subjects (n = 202). We found a significant difference in genotype frequencies among moderate and severe CCC patients with ventricular dysfunction. Conclusions: Our analysis suggests that the 118 rs2043055 polymorphism- or a SNP in tight linkage disequilibrium with it- may contribute to modulating the Chagas cardiomyopathy outcome.
- CD100 and plexins B2 and B1 mediate monocyte-endothelial cell adhesion and might take part in atherogenesis(2015) LUQUE, Maria Carolina A.; GUTIERREZ, Paulo S.; DEBBAS, Victor; KALIL, Jorge; STOLF, Beatriz S.Leukocyte migration is essential for the function of the immune system. Their recruitment from the vessels to the tissues involves sequential molecular interactions between leukocytes and endothelial cells (ECs). Many adhesion molecules involved in this process have already been described. However, additional molecules may be important in this interaction, and here we explore the potential role for CD100 and plexins in monocyte-EC binding. CD100 was shown to be involved in platelet-endothelial cell interaction, an important step in atherogenesis and thrombus formation. In a recent work we have described CD100 expression in monocytes and in macrophages and foam cells of human atherosclerotic plaques. In the present work, we have identified plexin B2 as a putative CD100 receptor in these cells. We have detected CD100 expression in the endothelium as well as in in vitro cultured endothelial cells. Blocking of CD 100, plexin B1 and/or B2 in adhesion experiments have shown that both CD100 and plexins act as adhesion molecules involved in monocyte-endothelial cell binding. This effect may be mediated by CD100 expressed in both cell types, probably coupled to the receptors endothelial plexin B1 and monocytic plexin B2. These results can bring new insights about a possible biological activity of CD100 in monocyte adhesion and atherosclerosis, as well as a future candidate for targeting therapeutics. (C) 2015 The Authors.