JORGE ELIAS KALIL FILHO

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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

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  • conferenceObject
    Descriptive Review of Clinical Data from 186 Records of Outpatients with IgA Deficiency Accompanied at a Quaternary Hospital in Brazil
    (2014) MENDONCA, L.; MASCARENHAS, F.; COHON, A.; KOKRON, C.; GRECCO, O.; KALIL, J.; BARROS, M.
  • article 3 Citação(ões) na Scopus
    Mycobacterium tuberculosis epitope-specific interferon-gamma production in healthy Brazilians reactive and non-reactive to tuberculin skin test
    (2014) SILVA, Bosco Christiano Maciel da; GRASSI, Maria Fernanda Rios; COUTINHO, Raimundo; MASCARENHAS, Rita Elizabeth Moreira; OLAVARRIA, Viviana Nilla; COUTINHO-BORGO, Adriana; KALIL, Jorge; CUNHA-NETO, Edecio; FONSECA, Simone Goncalves
    The interferon (IFN)-gamma response to peptides can be a useful diagnostic marker of Mycobacterium tuberculosis (MTB) latent infection. We identified promiscuous and potentially protective CD4(+) T-cell epitopes from the most conserved regions of MTB antigenic proteins by scanning the MTB antigenic proteins GroEL2, phosphate-binding protein 1 precursor and 19 kDa antigen with the TEPITOPE algorithm. Seven peptide sequences predicted to bind to multiple human leukocyte antigen (HLA)-DR molecules were synthesised and tested with IFN-gamma enzyme-linked immunospot (ELISPOT) assays using peripheral blood mononuclear cells (PBMCs) from 16 Mantoux tuberculin skin test (TST)-positive and 16 TST-negative healthy donors. Eighty-eight percent of TST-positive donors responded to at least one of the peptides, compared to 25% of TST-negative donors. Each individual peptide induced IFN-gamma production by PBMCs from at least 31% of the TST-positive donors. The magnitude of the response against all peptides was 182 +/- 230 x 10(6) IFN-gamma spot forming cells (SFC) among TST-positive donors and 36 +/- 62 x 10(6) SFC among TST-negative donors (p = 0.007). The response to GroEL2 (463-477) was only observed in the TST-positive group. This combination of novel MTB CD4 T-cell epitopes should be tested in a larger cohort of individuals with latent tuberculosis (TB) to evaluate its potential to diagnose latent TB and it may be included in ELISPOT-based IFN-gamma assays to identify individuals with this condition.
  • article 43 Citação(ões) na Scopus
    The CD8(+) Memory Stem T Cell (T-SCM) Subset Is Associated with Improved Prognosis in Chronic HIV-1 Infection
    (2014) RIBEIRO, Susan P.; MILUSH, Jeffrey M.; CUNHA-NETO, Edecio; KALLAS, Esper G.; KALIL, Jorge; SOMSOUK, Ma; HUNT, Peter W.; DEEKS, Steven G.; NIXON, Douglas F.; SENGUPTA, Devi
    Memory stem T cells (T-SCM) constitute a long-lived, self-renewing lymphocyte population essential for the maintenance of functional immunity. The hallmarks of HIV-1 pathogenesis are CD4(+) T cell depletion and abnormal cellular activation. We investigated the impact of HIV-1 infection on the T-SCM compartment, as well as any protective role these cells may have in disease progression, by characterizing this subset in a cohort of 113 subjects with various degrees of viral control on and off highly active antiretroviral therapy (HAART). We observed that the frequency of CD8(+) T-SCM was decreased in all individuals with chronic, untreated HIV-1 infection and that HAART had a restorative effect on this subset. In contrast, natural controllers of HIV-1 had the highest absolute number of CD4(+) T-SCM cells among all of the infected groups. The frequency of CD4(+) T-SCM predicted higher CD8(+) T-SCM frequencies, consistent with a role for the CD4(+) subset in helping to maintain CD8(+) memory T cells. In addition, T-SCM appeared to be progenitors for effector T cells (TEM), as these two compartments were inversely correlated. Increased frequencies of CD8(+) T-SCM predicted lower viral loads, higher CD4(+) counts, and less CD8(+) T cell activation. Finally, we found that T-SCM express the mucosal homing integrin alpha(4)beta(7) and can be identified in gut-associated lymphoid tissue (GALT). The frequency of mucosal CD4(+) T-SCM was inversely correlated with that in the blood, potentially reflecting the ability of these self-renewing cells to migrate to a crucial site of ongoing viral replication and CD4(+) T cell depletion. IMPORTANCE HIV-1 infection leads to profound impairment of the immune system. T-SCM constitute a recently identified lymphocyte subset with stem cell-like qualities, including the ability to generate other memory T cell subtypes, and are therefore likely to play an important role in controlling viral infection. We investigated the relationship between the size of the CD8(+) T-SCM compartment and HIV-1 disease progression in a cohort of chronically infected individuals. Our results suggest that HAART restores a normal frequency of CD8(+) T-SCM and that the natural preservation of this subset in the setting of untreated HIV-1 infection is associated with improved viral control and immunity. Therefore, the CD8(+) T-SCM population may represent a correlate of protection in chronic HIV-1 infection that is directly relevant to the design of T cell-based vaccines, adoptive immunotherapy approaches, or the pharmacologic induction of T-SCM.
  • article 51 Citação(ões) na Scopus
    Myocardial Gene Expression of T-bet, GATA-3, Ror-gamma t, FoxP3, and Hallmark Cytokines in Chronic Chagas Disease Cardiomyopathy: An Essentially Unopposed T(H)1-Type Response
    (2014) NOGUEIRA, Luciana Gabriel; SANTOS, Ronaldo Honorato Barros; FIORELLI, Alfredo Inacio; MAIRENA, Eliane Conti; BENVENUTI, Luiz Alberto; BOCCHI, Edimar Alcides; STOLF, Noedir Antonio; KALIL, Jorge; CUNHA-NETO, Edecio
    Background. Chronic Chagas disease cardiomyopathy (CCC), a late consequence of Trypanosoma cruzi infection, is an inflammatory cardiomyopathy with prognosis worse than those of noninflammatory etiology (NIC). Although the T cell-rich myocarditis is known to play a pathogenetic role, the relative contribution of each of the functional T cell subsets has never been thoroughly investigated. We therefore assessed gene expression of cytokines and transcription factors involved in differentiation and effector function of each functional T cell subset (T(H)1/T(H)2/T(H)17/Treg) in CCC, NIC, and heart donor myocardial samples. Methods and Results. Quantitative PCR showed markedly upregulated expression of IFN-gamma and transcription factor T-bet, and minor increases of GATA-3; FoxP3 and CTLA-4; IL-17 and IL-18 in CCC as compared with NIC samples. Conversely, cytokines expressed by T(H)2 cells (IL-4, IL-5, and IL-13) or associated with Treg (TGF-beta and IL-10) were not upregulated in CCC myocardium. Expression of T(H)1-related genes such as T-bet, IFN-gamma, and IL-18 correlated with ventricular dilation, FoxP3, and CTLA-4. Conclusions. Results are consistent with a strong local T(H)1-mediated response in most samples, possibly associated with pathological myocardial remodeling, and a proportionally smaller FoxP3(+)CTLA4(+) Treg cell population, which is unable to completely curb IFN-gamma production in CCC myocardium, therefore fueling inflammation.
  • article 3 Citação(ões) na Scopus
    Drug-induced anaphylaxis in children: Nonsteroidal anti-inflammatory drugs and drug provocation test REPLY
    (2014) AUN, Marcelo Vivolo; BLANCA, Miguel; GARRO, Laila Sabino; RIBEIRO, Marisa Rosimeire; KALIL, Jorge; MOTTA, Antonio Abilio; CASTELLS, Mariana; GIAVINA-BIANCHI, Pedro
  • article 12 Citação(ões) na Scopus
    Short Communication: HIV Type 1 Subtype BF Leads to Faster CD4(+) T Cell Loss Compared to Subtype B
    (2014) TAROSSO, Leandro F.; SANABANI, Sabri S.; RIBEIRO, Susan P.; SAUER, Mariana M.; TOMIYAMA, Helena I.; SUCUPIRA, Maria C.; DIAZ, Ricardo S.; SABINO, Ester C.; KALIL, Jorge; KALLAS, Esper G.
    Although it has been suggested that biological differences among HIV-1 subtypes exist, their possible influence on disease progression has not been fully revealed. In particular, the increasing emergence of recombinants stresses the need to characterize disease presentation in persons infected by these diverse HIV-1 forms. We explored this issue among 83 Brazilian subjects infected with either HIV-1 subtype B or recombinant subtype BF, all followed since incident infection in a cohort study. Viral subtypes were assigned by full length sequencing of HIV-1 genomes. We observed that the baseline measures for CD4(+) T cells and viral load did not differ between the groups. However, longitudinal analysis revealed that subtype BF was clearly associated with a faster CD4(+) T cell decline compared to infection with subtype B, in spite of a similar plasma HIV-1 load. While subtype B-infected subjects presented a loss of 3.6 CD4(+) T cells/l per month, subtype BF-infected individuals showed a monthly decay of 6.3 CD4(+) T cells/l (p<0.01). The time to reach 350 CD4(+) T cells/l and the time to start antiretroviral treatment were also shorter in subtype BF-infected persons. The elucidation of an accelerated CD4(+) T cell loss associated with subtype BF suggests that this HIV-1 genetic form could be more pathogenic than subtype B.
  • conferenceObject
    Complement Activation in a Group of Patients with IGG 4 Related Disease at Hospital Das Clincas - University of Sao Paulo
    (2014) MENDONCA, L.; MASCARENHAS, F.; KOKRON, C.; KALIL, J.; BARROS, M.
  • conferenceObject
    Aerobic training decrease bronchial hyperresponsiveness and systemic inflammation in patients with moderate or severe asthma: A randomized controlled trial
    (2014) CARVALHO, Celso R. F.; FRANCA-PINTO, Andrezza; MENDES, Felipe A. R.; STELMACH, Rafael; CUKIER, Alberto; AGONDI, Rosana C.; MARTINS, Milton A.; SARAIVA-ROMANHOLO, Beatriz M.; KALIL, Jorge; GIAVINA-BIANCHI, Pedro
  • conferenceObject
    Role of Autoimmunity in Hepatitis C Virus Infection: A Case Report and a Brief Review of Literature
    (2014) LIMA, F. M. S.; MENDONCA, L. O.; KOKRON, C. M.; KALIL, J.; CORDOVA, P. T.; BARROS, M. T.
  • article 82 Citação(ões) na Scopus
    MicroRNAs miR-1, miR-133a, miR-133b, miR-208a and miR-208b are dysregulated in Chronic Chagas disease Cardiomyopathy
    (2014) FERREIRA, Ludmila Rodrigues Pinto; FRADE, Amanda Farage; SANTOS, Ronaldo Honorato Barros; TEIXEIRA, Priscila Camillo; BARON, Monique Andrade; NAVARRO, Isabela Cunha; BENVENUTI, Luiz Alberto; FIORELLI, Alfredo Inacio; BOCCHI, Edimar Alcides; STOLF, Noedir Antonio; CHEVILLARD, Christophe; KALIL, Jorge; CUNHA-NETO, Edecio
    Background/methods: Chagas disease is caused by an intracellular parasite, Trypanosoma cruzi, and it is a leading cause of heart failure in Latin America. The main clinical consequence of the infection is the development of a Chronic Chagas disease Cardiomyopathy (CCC), which is characterized by myocarditis, hypertrophy and fibrosis and affects about 30% of infected patients. CCC has a worse prognosis than other cardiomyopathies, like idiopathic dilated cardiomyopathy (DCM). It is well established that myocardial gene expression patterns are altered in CCC, but the molecular mechanisms underlying these differences are not clear. MicroRNAs are recently discovered regulators of gene expression, and are recognized as important factors in heart development and cardiovascular disorders (CD). We analyzed the expression of nine different miRNAs inmyocardial tissue samples of CCC patients in comparison to DCM patients and samples from heart transplant donors. Using the results of a cDNA microarray database on CCC and DCM myocardium, signaling networks were built and nodal molecules were identified. Results: We observed that five miRNAs were significantly altered in CCC and three in DCM; importantly, three miRNAs were significantly reduced in CCC as compared to DCM. We observed that multiple gene targets of the differentially expressed miRNAs showed a concordant inverse expression in CCC. Significantly, most gene targets and involved networks belong to crucial disease-related signaling pathways. Conclusion: These results suggest that miRNAs may play a major role in the regulation of gene expression in CCC pathogenesis, with potential implication as diagnostic and prognostic tools.