Bruna Cunha de Alencar

@usp.br

Assistent Professor, Department of Immunology
Instituto de Ciencias Biomedicas / Universidade de Sao Paulo

Bruna Cunha de Alencar


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https://researchid.co/bruna.alencar

EDUCATION

Bachelor in Biomedical Sciences
PhD in Immunology and Microbiology
Post-doctorate in Virology

RESEARCH INTERESTS

Immunology
Cell Biology
Virology
HIV
27

Scopus Publications

1425

Scholar Citations

20

Scholar h-index

22

Scholar i10-index

Scopus Publications

  • Macrophage Protein Disulfide Isomerase Increases Infection by Leishmania amazonensis
    Guilherme M. P. Carrara, Guilherme A. Souza‐Silva, Tania C. B. d. Reis, Bruna C. d. Alencar, Silvia B. Boscardin, et al.
    Cell Biology International, 2025
    Leishmania spp. are protozoans with a digenetic life cycle responsible for causing tegumentary and visceral leishmaniasis. Leishmania (L.) amazonensis is the second most prevalent dermotropic species in Brazil. Infection in humans and other mammals takes place when phagocytes, mainly macrophages, uptake the parasite. Many proteins on the phagocytic cell surface participate in Leishmania phagocytosis. In this study, we evaluated the role of surface protein disulfide isomerase (PDI) in phagocytosis and infection of macrophages by L. amazonensis. PDI is the second most abundant chaperone in the endoplasmic reticulum. A unique study in the literature associated the presence of PDI on the macrophage surface with increased phagocytosis by Leishmania (L.) infantum (syn L. chagasi), the species most frequently associated with visceral leishmaniasis in the Americas. In the present work we evaluated L. amazonensis infections in transgenic FVB/NJ mice overexpressing PDI (TgPDIA1). We validated the presence of PDI on their macrophages surface by flow cytometry. We demonstrated that infection of macrophages pretreated with anti‐PDI antibodies was lower compared to control cells. Accordingly, we showed that the overexpression of PDI increased the adhesion of parasites and infection of macrophages. We also demonstrated that macrophages overexpressing PDI internalize more zymosan particles. In vivo imaging of infections with luciferase‐expressing parasites in wild‐type and TgPDIA1 mice indicated that the overexpression of PDI was not associated with significant differences in footpad lesions and parasite burden, probably due to the ubiquitous overexpression of PDI and the roles of this molecule in other immune system functions.
  • Leishmania (Leishmania) amazonensis and Leishmania (Leishmania) infantum sialic acids enhance macrophage infection
    Tainá Cavalcante, Antônio Moreira Marques, Mariana Medina Medeiros, Tania Carolina Reis, Daniel Quina, et al.
    Cell Biology International, 2025
    Leishmaniases affect millions of people around the world, caused by Leishmania parasites. Leishmania are transmitted by female sandflies from Phlebotominae subfamily during their blood meals. In mammals, promastigotes are phagocytosed mainly by macrophages, differentiate into amastigotes and multiply. For entry and survival in macrophages, Leishmania uses virulence factors such as surface glycoconjugates. Sialic acids (Sias) are found in terminal portions of glycoconjugates and play important roles in human pathogens. The importance of Sias was explored only in L. (L.) donovani, associated with visceral leishmaniasis in Africa, Asia and Europe. Thus, the aim of this study was to characterize Sias of Leishmania (L.) amazonensis and Leishmania (L.) infantum, related to cutaneous and visceral leishmaniasis in South America, respectively. For that, we analyzed by HPLC‐FLD the Sias of promastigotes of L. (L.) amazonensis LV79 and two L. (L.) infantum strains, and of L. (L.) amazonensis axenic amastigotes and amastigotes from paw lesions of infected mice. To evaluate Sias importance in promastigotes, we treated stationary phase parasites with sialidase and infected murine and human macrophages. We detected N‐Acetylneuraminic Acid in promastigotes of all strains, with greater abundance in L. (L.) infantum. We identified N‐Acetylneuraminic Acid and N‐Glycolylneuraminic acid in amastigotes recovered from paw lesion, but only N‐Acetylneuraminic Acid in axenic amastigotes. Promastigotes treated with sialidase infected less macrophages than parasites displaying total Sias. Our results demonstrate that Sias vary between Leishmania species and between L. (L.) amazonensis life stages and plays an important role in macrophage infection by L. (L.) amazonensis and L. (L.) infantum.
  • Myosin IXB protects immune cells from virus infection
    Leticia Kogachi, Taís Matozo, Yuli Thamires Magalhães, Marina Janoni Bayerlein, Tania Carolina Braga, et al.
    Journal of General Virology, 2025
    Actin-associated proteins have been implicated in several stages of virus infection. However, the role of myosins, which are actin-dependent molecular motors, during virus infection and pathogenesis is poorly understood. Myosin IXB (Myo9b) is a member of the myosin family abundantly expressed in immune cells. Myo9b displays a RhoGTPase-activating protein domain capable of modulating actin dynamics by inhibiting RhoGTPase activity. To enquire upon Myo9b participation in virus infections, we have silenced Myo9b in U937 and Jurkat cells and infected them with vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped HIV-1. Myo9b-silenced U937 showed a remarkable increase of above ten times more HIV-VSV-G infection than control cells. We observed a similar pattern in Jurkat cell infection with both WT Env and VSV-G-pseudotyped HIV, albeit to a lesser extent. Myo9b-silenced U937 cells presented elevated levels of phosphorylated cofilin, but lower levels of polymerized actin. The use of a RhoA, B and C inhibitor, as well as a Rac1 inhibitor, reduced virus infection. Finally, we have also observed an increment in virus internalization and fusion in cells knockdown for Myo9b, which may explain the increase in virus infection. Taken together, our data suggests that Myo9b might hinder viral entry and infection by controlling the activity of RhoGTPases in immune cells.
  • Myosin motors on the pathway of viral infections
    Tais Matozo, Leticia Kogachi, Bruna Cunha de Alencar
    Cytoskeleton, 2022
    Molecular motors are microscopic machines that use energy from ATP hydrolysis to generate movement. While kinesins and dynein are molecular motors associated with microtubule tracks, myosins bind to and move on actin filaments. Mammalian cells express several myosin motors. They power cellular processes such as endo- and exocytosis, intracellular trafficking, transcription, migration, and cytokinesis. As viruses navigate through cells, they may take advantage or be hindered by host components and machinery, including the cytoskeleton. This review delves into myosins' cell roles and compares them to their reported functions in viral infections. In most cases, the previously described myosin functions align with their reported role in viral infections, although not in all cases. This opens the possibility that knowledge obtained from studying myosins in viral infections might shed light on new physiological roles for myosins in cells. However, given the high number of myosins expressed and the variety of viruses investigated in the different studies, it is challenging to infer whether the interactions found are specific to a single virus or can be applied to other viruses with the same characteristics. We conclude that the participation of myosins in viral cycles is still a largely unexplored area, especially concerning unconventional myosins. This article is protected by copyright. All rights reserved.
  • Antiviral Response Induced by Toll-Like Receptor (TLR) 7/TLR8 Activation Inhibits Human Immunodeficiency Virus Type 1 Infection in Cord Blood Macrophages
    Anna J Pietrobon, Fábio S Y Yoshikawa, Luana M Oliveira, Natalli Z Pereira, Tais Matozo, et al.
    Journal of Infectious Diseases, 2022
    Vertical transmission is the main mechanism of human immunodeficiency virus type 1 (HIV-1) infection in infants, who may develop high viremia and rapidly progress to AIDS. Innate immunity agonists can control HIV-1 replication in vitro, but the protective effect in the neonatal period remains unknown. Herein, we evaluated the immunomodulatory and antiviral effects of type I interferon (IFN-I) adjuvants on cord blood monocyte-derived macrophages upon HIV-1 infection. Despite the phenotypic and transcriptional similarities between cord blood and adult macrophages, cord blood cells were prone to viral replication when infected with HIV-1. However, treatment with CL097 efficiently promoted the antiviral and inflammatory responses and inhibited HIV-1 replication in cord blood cells in an NF-κB and autophagy activation-independent manner. Our data suggest that cord blood macrophages are able to establish antiviral responses induced by IFN-I adjuvants similar to those of their adult counterparts, revealing a potential adjuvant candidate to enhance the neonatal immune response.
  • Flagellin/NLRC4 pathway rescues NLRP3-inflammasome defect in dendritic cells from HIV-infected patients: Perspective for new adjuvant in immunocompromised individuals
    Edione Cristina dos Reis, Vinícius Nunes Cordeiro Leal, Jaíne Lima da Silva Soares, Fernanda Pereira Fernandes, Dhêmerson Souza de Lima, et al.
    Frontiers in Immunology, 2019
    Introduction: NLRP3 inflammasome plays a key role in dendritic cells (DC) activation in response to vaccine adjuvants, however we previously showed that it is not properly activated in DC from HIV-infected patients (HIV-DC), explaining, at least in part, the poor response to immunization of these patients. Taking in account that several cytoplasmic receptors are able to activate inflammasome, and that bacterial components are considered as a novel and efficient adjuvant, we postulated that bacterial flagellin (FLG), a natural ligand of NAIP/NLRC4 inflammasome, could rescue the activation of the complex in HIV-DC. Objective: Demonstrate that FLG is able to activate monocyte-derived dendritic cells from HIV-infected individuals better than LPS, and to what extent the entity of inflammasome activation differs between DC from HIV-infected patients and healthy donors. Methods: Monocyte-derived dendritic cells from HIV-infected patients (HIV-DC) and healthy donors (HD-DC) were stimulated with FLG, and inflammasome as well as DC activation (phenotypic profile, cytokine production, autologous lymphocytes activation) were compared. Chemical and genetic inhibitors were used to depict the relative contribution of NLRC4 and NLRP3 in HIV/HD-DC response to FLG. Results: FLG properly activates HD-DC and HIV-DC. FLG induces higher inflammasome activation than LPS in HIV-DC. FLG acts through NLRC4 and NLRP3 in HD-DC, but at a lesser extent in HIV-DC due to intrinsic NLRP3 defect. Conclusions: FLG by-passes NLRP3 defect in HIV-DC, through the activation of NAIP/NLRC4 inflammasome, indicating possible future use of the bacterial component as an efficient adjuvant in immunocompromised individuals.
  • Polymorphisms in SIGLEC1 contribute to susceptibility to pulmonary active tuberculosis possibly through the modulation of IL-1ß
    Dhemerson Souza de Lima, Vinicius C.L. Nunes, Mauricio M. Ogusku, Aya Sadahiro, Alessandra Pontillo, et al.
    Infection Genetics and Evolution, 2017
    Siglec-1/CD169 is a sialoadhesin expressed by macrophages thought to function in cell-to-cell interactions. In the lung, the expression of Siglec-1 is specific for alveolar macrophages and single nucleotide polymorphisms (SNPs) in SIGLEC1 have been recently associated with asthma severity. Taking in account the role of alveolar macrophages in the control of M. tuberculosis and the poor literature about the contribution of SIGLEC1 genetics in M. tuberculosis susceptibility and development of pulmonary active TB, selected SNPs in SIGLEC1 were analysed in a case/control cohort from a TB endemic area of Brazil Amazon. Our findings evidenced for the first time the novel association between SIGLEC1 rs3859664 SNP and active pulmonary TB. Intriguingly, carriers of the polymorphism produced less IL-1ß than non-carriers, suggesting the possible involvement of Siglec-1 signalling pathway with inflammasome complex.
  • Sensing of HIV-1 entry triggers a type I interferon response in human primary macrophages
    Jérémie Decalf, Marion Desdouits, Vasco Rodrigues, François-Xavier Gobert, Matteo Gentili, et al.
    Journal of Virology, 2017
    Along with CD4+ T lymphocytes, macrophages are a major cellular source of HIV-1 replication and a potential viral reservoir. Following entry and reverse transcription in macrophages, cloaking of the viral cDNA by the HIV-1 capsid limits its cytosolic detection, enabling efficient replication. However, whether incoming HIV-1 particles are sensed by macrophages prior to reverse transcription remains unclear. Here, we show that HIV-1 triggers a broad expression of interferon (IFN)-stimulated genes (ISG) in monocyte-derived macrophages within a few hours after infection. This response does not require viral reverse transcription or the presence of HIV-1 RNA within particles, but viral fusion is essential. This response is elicited by viruses carrying different envelope proteins and thus different receptors to proceed for viral entry. Expression of ISG in response to viral entry requires TBK1 activity and type I IFNs signaling. Remarkably, the ISG response is transient but affects subsequent viral spread. Together, our results shed light on an early step of HIV-1 sensing by macrophages at the level of entry, which confers an early protection through type I IFN signaling and has potential implications in controlling the infection. IMPORTANCE HIV infection is restricted to T lymphocytes and macrophages. HIV-1-infected macrophages are found in many tissues of infected patients, even under antiretroviral therapy, and are considered a viral reservoir. How HIV-1 is detected and what type of responses are elicited upon sensing remain in great part elusive. The kinetics and localization of the production of cytokines such as interferons in response to HIV is of critical importance to understanding how the infection and the immune response are established. Our study provides evidence that macrophages can detect HIV-1 as soon as it enters the cell. Interestingly, this sensing is independent of the presence of viral nucleic acids within the particles but requires their fusion with the macrophages. This triggers a low interferon response, which activates an antiviral program protecting cells against further viral challenge and thus potentially limiting the spread of the infection.
  • HIV trafficking in host cells: Motors wanted!
    Raphaël Gaudin, Bruna Cunha de Alencar, Nathalie Arhel, Philippe Benaroch
    Trends in Cell Biology, 2013
    Throughout the viral replication cycle, viral proteins, complexes, and particles need to be transported within host cells. These transport events are dependent on the host cell cytoskeleton and molecular motors. However, the mechanisms by which virus is trafficked along cytoskeleton filaments and how molecular motors are recruited and regulated to guarantee successful integration of the viral genome and production of new viruses has only recently begun to be understood. Recent studies on HIV have identified specific molecular motors involved in the trafficking of these viral particles. Here we review recent literature on the transport of HIV components in the cell, provide evidence for the identity and role of molecular motors in this process, and highlight how these trafficking events may be related to those occurring with other viruses.
  • CD36-specific antibodies block release of HIV-1 from infected primary macrophages and its transmission to T cells
    Stefano Berre, Raphaël Gaudin, Bruna Cunha de Alencar, Marion Desdouits, Mélanie Chabaud, et al.
    Journal of Experimental Medicine, 2013
    HIV-1–infected macrophages likely represent viral reservoirs, as they accumulate newly formed virions in internal virus-containing compartments (VCCs). However, the nature and biogenesis of VCCs remain poorly defined. We show that upon HIV-1 infection of primary human macrophages, Gag is recruited to preexisting compartments containing the scavenger receptor CD36, which then become VCCs. Silencing of CD36 in HIV-1–infected macrophages decreases the amount of virions released. Strikingly, soluble anti-CD36 antibodies, but not the natural ligands of CD36, inhibit release of virions from HIV-1–infected macrophages and the transmission of virus to CD4+ T cells. The effect of the antibodies is potent, rapid, and induces the retention of virions within VCCs. Ectopic expression of CD36 in HeLa cells renders them susceptible to the inhibitory effect of the anti-CD36 mAb upon HIV-1 infection. We show that the anti-CD36 mAb inhibits HIV-1 release by clustering newly formed virions at their site of budding, and that signaling via CD36 is not required. Thus, HIV-1 reservoirs in macrophages may be tackled therapeutically using anti-CD36 antibodies to prevent viral dissemination.
  • Dynamics of HIV-Containing Compartments in Macrophages Reveal Sequestration of Virions and Transient Surface Connections
    Raphaël Gaudin, Stefano Berre, Bruna Cunha de Alencar, Jérémie Decalf, Michael Schindler, et al.
    Plos One, 2013
  • Critical role for the kinesin KIF3A in the HIV life cycle in primary human macrophages
    Raphaël Gaudin, Bruna Cunha de Alencar, Mabel Jouve, Stefano Bèrre, Emmanuel Le Bouder, et al.
    Journal of Cell Biology, 2012
  • Pathogen-induced proapoptotic phenotype and high CD95 (Fas) expression accompany a suboptimal CD8+ T-cell response: Reversal by adenoviral vaccine
    José Ronnie Vasconcelos, Oscar Bruña–Romero, Adriano F. Araújo, Mariana R. Dominguez, Jonatan Ersching, et al.
    Plos Pathogens, 2012
  • Acquired immunity against trypanosoma cruzi infection and vaccine development
    Emerging Chagas Disease, 2011
  • Subdominant/cryptic CD8 T cell epitopes contribute to resistance against experimental infection with a human protozoan parasite
    Mariana R. Dominguez, Eduardo L. V. Silveira, José Ronnie C. de Vasconcelos, Bruna C. G. de Alencar, Alexandre V. Machado, et al.
    Plos One, 2011
  • Heterologous plasmid DNA prime-recombinant human adenovirus 5 boost vaccination generates a stable pool of protective long-lived CD8+ T effector memory cells specific for a human parasite, Trypanosoma cruzi
    Paula Ordonhez Rigato, Bruna C. de Alencar, José Ronnie C. de Vasconcelos, Mariana R. Dominguez, Adriano F. Araújo, et al.
    Infection and Immunity, 2011
  • CD8+ T cell adjuvant effects of Salmonella FliCd flagellin in live vaccine vectors or as purified protein
    Catarina J.M. Braga, Liliana M. Massis, Maria E. Sbrogio-Almeida, Bruna C.G. Alencar, Daniel Y. Bargieri, et al.
    Vaccine, 2010
  • Impaired innate immunity in Tlr4-/- mice but preserved CD8+ T cell responses against trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or myd88-deficient mice
    Ana-Carolina Oliveira, Bruna C. de Alencar, Fanny Tzelepis, Weberton Klezewsky, Raquel N. da Silva, et al.
    Plos Pathogens, 2010
  • Perforin and gamma interferon expression are required for CD4+ and CD8+ T-cell-dependent protective immunity against a human parasite, Trypanosoma cruzi, elicited by heterologous plasmid DNA prime-recombinant adenovirus 5 boost vaccination
    Bruna C. G. de Alencar, Pedro M. Persechini, Filipe A. Haolla, Gabriel de Oliveira, Jaline C. Silverio, et al.
    Infection and Immunity, 2009
  • Strain-specific protective immunity following vaccination against experimental Trypanosoma cruzi infection
    Filipe A. Haolla, Carla Claser, Bruna C.G. de Alencar, Fanny Tzelepis, José Ronnie de Vasconcelos, et al.
    Vaccine, 2009
  • Immunodominance: A new hypothesis to explain parasite escape and host/parasite equilibrium leading to the chronic phase of Chagas' disease?
    M.M. Rodrigues, B.C.G. de Alencar, C. Claser, F. Tzelepis
    Brazilian Journal of Medical and Biological Research, 2009
  • Swimming against the current: Genetic vaccination against Trypanosoma cruzi infection in mice
    Mauricio M Rodrigues, Bruna C de Alencar, Carla Claser, Fanny Tzelepis, Eduardo L Silveira, et al.
    Memorias do Instituto Oswaldo Cruz, 2009
  • Infection with Trypanosoma cruzi restricts the repertoire of parasite-specific CD8+ T cells leading to immunodominance
    Fanny Tzelepis, Bruna C. G. de Alencar, Marcus L. O. Penido, Carla Claser, Alexandre V. Machado, et al.
    Journal of Immunology, 2008
  • Cytotoxic T cell adjuvant effects of three Salmonella enterica flagellins
    Catarina J.M. Braga, Liliana M. Massis, Bruna C.G. Alencar, Maurício M. Rodrigues, M.E. Sbrogio-Almeida, et al.
    Brazilian Journal of Microbiology, 2008
  • Cross-priming of long lived protective CD8+ T cells against Trypanosoma cruzi infection: Importance of a TLR9 agonist and CD4+ T cells
    Bruna C.G. de Alencar, Adriano F.S. Araújo, Marcus L.O. Penido, Ricardo T. Gazzinelli, Mauricio M. Rodrigues
    Vaccine, 2007

RECENT SCHOLAR PUBLICATIONS

  • Macrophage Protein Disulfide Isomerase Increases Infection by Leishmania amazonensis
    GMP Carrara, GA Souza‐Silva, TCB Reis, BC Alencar, SB Boscardin, ...
    Cell Biology International , 2025
    2025
    Citations: 1
  • Myosin IXB protects immune cells from virus infection
    L Kogachi, T Matozo, YT Magalhães, M Janoni Bayerlein, TC Braga, ...
    Journal of General Virology 106 (4), 002090 , 2025
    2025
    Citations: 1
  • Leishmania (Leishmania) amazonensis and Leishmania (Leishmania) infantum sialic acids enhance macrophage infection
    T Cavalcante, AM Marques, MM Medeiros, TC Reis, D Quina, ...
    Cell Biology International , 2025
    2025
  • Antiviral Response Induced by Toll-Like Receptor (TLR) 7/TLR8 Activation Inhibits Human Immunodeficiency Virus Type 1 Infection in Cord Blood Macrophages
    AJ Pietrobon, FSY Yoshikawa, LM Oliveira, NZ Pereira, T Matozo, ...
    The Journal of Infectious Diseases 225 (3), 510-519 , 2022
    2022
    Citations: 8
  • Myosin motors on the pathway of viral infections
    T Matozo, L Kogachi, BC de Alencar
    Cytoskeleton 79 (6-8), C1, 41-63 , 2022
    2022
    Citations: 16
  • Flagellin/NLRC4 Pathway Rescues NLRP3-Inflammasome Defect in Dendritic Cells From HIV-Infected Patients: Perspective for New Adjuvant in Immunocompromised Individuals
    PA Dos Reis EC, Leal VNC, Soares JLS, Fernandes FP, Souza de Lima D, de ...
    Frontiers in Immunology , 2019
    2019
    Citations: 36
  • Polymorphisms in SIGLEC1 contribute to susceptibility to pulmonary active tuberculosis possibly through the modulation of IL-1ß.
    D Souza de Lima, VCL Nunes, MM Ogusku, A Sadahiro, A Pontillo, ...
    Infection, Genetics and Evolution 55, 313-317 , 2017
    2017
    Citations: 20
  • Sensing of HIV-1 entry triggers a type I interferon response in human primary macrophages
    J Decalf, M Desdouits, V Rodrigues, FX Gobert, M Gentili, ...
    Journal of virology 91 (15), 10.1128/jvi. 00147-17 , 2017
    2017
    Citations: 56
  • HIV trafficking in host cells: motors wanted!
    R Gaudin, BC de Alencar, N Arhel, P Benaroch
    Trends in cell biology 23 (12), 652-662 , 2013
    2013
    Citations: 75
  • CD36-specific antibodies block release of HIV-1 from infected primary macrophages and its transmission to T cells
    S Berre, R Gaudin, B Cunha de Alencar, M Desdouits, M Chabaud, ...
    Journal of Experimental Medicine 210 (12), 2523-2538 , 2013
    2013
    Citations: 63
  • Dynamics of HIV-containing compartments in macrophages reveal sequestration of virions and transient surface connections
    R Gaudin, S Berre, B Cunha de Alencar, J Decalf, M Schindler, FX Gobert, ...
    PloS one 8 (7), e69450 , 2013
    2013
    Citations: 83
  • Critical role for the kinesin KIF3A in the HIV life cycle in primary human macrophages
    R Gaudin, B Cunha de Alencar, M Jouve, S Bèrre, E Le Bouder, ...
    Journal of Cell Biology 199 (3), 467-479 , 2012
    2012
    Citations: 62
  • Pathogen-Induced Proapoptotic Phenotype and High CD95 (Fas) Expression Accompany a Suboptimal CD8 + T-Cell Response: Reversal by Adenoviral Vaccine
    JR Vasconcelos, O Bruña–Romero, AF Araujo, MR Dominguez, ...
    PLoS pathogens 8 (5), e1002699 , 2012
    2012
    Citations: 74
  • Subdominant/cryptic CD8 T cell epitopes contribute to resistance against experimental infection with a human protozoan parasite
    MR Dominguez, ELV Silveira, JRC de Vasconcelos, BCG de Alencar, ...
    PloS one 6 (7), e22011 , 2011
    2011
    Citations: 64
  • Heterologous plasmid DNA prime-recombinant human adenovirus 5 boost vaccination generates a stable pool of protective long-lived CD8+ T effector memory cells specific for a …
    PO Rigato, BC de Alencar, JRC de Vasconcelos, MR Dominguez, ...
    Infection and immunity 79 (5), 2120-2130 , 2011
    2011
    Citations: 74
  • Acquired immunity against Trypanosoma cruzi infection and vaccine development
    MM Rodrigues, BC de Alencar, JR Vasconcelos
    Emerging Chagas Disease, 94 , 2011
    2011
    Citations: 1
  • Impaired Innate Immunity in Tlr4 −/− Mice but Preserved CD8 + T Cell Responses against Trypanosoma cruzi in Tlr4 -, Tlr2 -, Tlr9 - or Myd88 -Deficient Mice
    AC Oliveira, BC De Alencar, F Tzelepis, W Klezewsky, RN da Silva, ...
    PLoS pathogens 6 (4), e1000870 , 2010
    2010
    Citations: 84
  • CD8 + T cell adjuvant effects of Salmonella FliC d flagellin in live vaccine vectors or as purified protein
    CJM Braga, LM Massis, ME Sbrogio-Almeida, BCG Alencar, DY Bargieri, ...
    Vaccine 28 (5), 1373-1382 , 2010
    2010
    Citations: 69
  • Perforin and gamma interferon expression are required for CD4+ and CD8+ T-cell-dependent protective immunity against a human parasite, Trypanosoma cruzi, elicited by …
    BCG de Alencar, PM Persechini, FA Haolla, G de Oliveira, JC Silverio, ...
    Infection and immunity 77 (10), 4383-4395 , 2009
    2009
    Citations: 127
  • Strain-specific protective immunity following vaccination against experimental Trypanosoma cruzi infection
    FA Haolla, C Claser, BCG de Alencar, F Tzelepis, JR de Vasconcelos, ...
    Vaccine 27 (41), 5644-5653 , 2009
    2009
    Citations: 58

MOST CITED SCHOLAR PUBLICATIONS

  • Perforin and gamma interferon expression are required for CD4+ and CD8+ T-cell-dependent protective immunity against a human parasite, Trypanosoma cruzi, elicited by …
    BCG de Alencar, PM Persechini, FA Haolla, G de Oliveira, JC Silverio, ...
    Infection and immunity 77 (10), 4383-4395 , 2009
    2009
    Citations: 127
  • Distinct kinetics of effector CD8+ cytotoxic T cells after infection with Trypanosoma cruzi in naive or vaccinated mice
    F Tzelepis, BCG de Alencar, MLO Penido, RT Gazzinelli, PM Persechini, ...
    Infection and immunity 74 (4), 2477-2481 , 2006
    2006
    Citations: 123
  • Infection with Trypanosoma cruzi restricts the repertoire of parasite-specific CD8+ T cells leading to immunodominance
    F Tzelepis, BCG de Alencar, MLO Penido, C Claser, AV Machado, ...
    The Journal of Immunology 180 (3), 1737-1748 , 2008
    2008
    Citations: 108
  • CD8+-T-cell-dependent control of Trypanosoma cruzi infection in a highly susceptible mouse strain after immunization with recombinant proteins based on amastigote surface protein 2
    AFS Araújo, BCG de Alencar, JRC Vasconcelos, MI Hiyane, CRF Marinho, ...
    Infection and immunity 73 (9), 6017-6025 , 2005
    2005
    Citations: 98
  • Impaired Innate Immunity in Tlr4 −/− Mice but Preserved CD8 + T Cell Responses against Trypanosoma cruzi in Tlr4 -, Tlr2 -, Tlr9 - or Myd88 -Deficient Mice
    AC Oliveira, BC De Alencar, F Tzelepis, W Klezewsky, RN da Silva, ...
    PLoS pathogens 6 (4), e1000870 , 2010
    2010
    Citations: 84
  • Dynamics of HIV-containing compartments in macrophages reveal sequestration of virions and transient surface connections
    R Gaudin, S Berre, B Cunha de Alencar, J Decalf, M Schindler, FX Gobert, ...
    PloS one 8 (7), e69450 , 2013
    2013
    Citations: 83
  • HIV trafficking in host cells: motors wanted!
    R Gaudin, BC de Alencar, N Arhel, P Benaroch
    Trends in cell biology 23 (12), 652-662 , 2013
    2013
    Citations: 75
  • Pathogen-Induced Proapoptotic Phenotype and High CD95 (Fas) Expression Accompany a Suboptimal CD8 + T-Cell Response: Reversal by Adenoviral Vaccine
    JR Vasconcelos, O Bruña–Romero, AF Araujo, MR Dominguez, ...
    PLoS pathogens 8 (5), e1002699 , 2012
    2012
    Citations: 74
  • Heterologous plasmid DNA prime-recombinant human adenovirus 5 boost vaccination generates a stable pool of protective long-lived CD8+ T effector memory cells specific for a …
    PO Rigato, BC de Alencar, JRC de Vasconcelos, MR Dominguez, ...
    Infection and immunity 79 (5), 2120-2130 , 2011
    2011
    Citations: 74
  • CD8 + T cell adjuvant effects of Salmonella FliC d flagellin in live vaccine vectors or as purified protein
    CJM Braga, LM Massis, ME Sbrogio-Almeida, BCG Alencar, DY Bargieri, ...
    Vaccine 28 (5), 1373-1382 , 2010
    2010
    Citations: 69
  • Subdominant/cryptic CD8 T cell epitopes contribute to resistance against experimental infection with a human protozoan parasite
    MR Dominguez, ELV Silveira, JRC de Vasconcelos, BCG de Alencar, ...
    PloS one 6 (7), e22011 , 2011
    2011
    Citations: 64
  • CD36-specific antibodies block release of HIV-1 from infected primary macrophages and its transmission to T cells
    S Berre, R Gaudin, B Cunha de Alencar, M Desdouits, M Chabaud, ...
    Journal of Experimental Medicine 210 (12), 2523-2538 , 2013
    2013
    Citations: 63
  • Critical role for the kinesin KIF3A in the HIV life cycle in primary human macrophages
    R Gaudin, B Cunha de Alencar, M Jouve, S Bèrre, E Le Bouder, ...
    Journal of Cell Biology 199 (3), 467-479 , 2012
    2012
    Citations: 62
  • Strain-specific protective immunity following vaccination against experimental Trypanosoma cruzi infection
    FA Haolla, C Claser, BCG de Alencar, F Tzelepis, JR de Vasconcelos, ...
    Vaccine 27 (41), 5644-5653 , 2009
    2009
    Citations: 58
  • Sensing of HIV-1 entry triggers a type I interferon response in human primary macrophages
    J Decalf, M Desdouits, V Rodrigues, FX Gobert, M Gentili, ...
    Journal of virology 91 (15), 10.1128/jvi. 00147-17 , 2017
    2017
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  • Cross-priming of long lived protective CD8+ T cells against Trypanosoma cruzi infection: importance of a TLR9 agonist and CD4+ T cells
    BCG de Alencar, AFS Araújo, MLO Penido, RT Gazzinelli, MM Rodrigues
    Vaccine 25 (32), 6018-6027 , 2007
    2007
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  • Flagellin/NLRC4 Pathway Rescues NLRP3-Inflammasome Defect in Dendritic Cells From HIV-Infected Patients: Perspective for New Adjuvant in Immunocompromised Individuals
    PA Dos Reis EC, Leal VNC, Soares JLS, Fernandes FP, Souza de Lima D, de ...
    Frontiers in Immunology , 2019
    2019
    Citations: 36
  • Immunodominance: a new hypothesis to explain parasite escape and host/parasite equilibrium leading to the chronic phase of Chagas' disease?
    MM Rodrigues, BCG de Alencar, C Claser, F Tzelepis
    Brazilian Journal of Medical and Biological Research 42, 220-223 , 2009
    2009
    Citations: 35
  • Cytotoxic T cell adjuvant effects of three Salmonella enterica flagellins
    CJM Braga, LM Massis, BCG Alencar, MM Rodrigues, ...
    Brazilian Journal of Microbiology 39, 44-49 , 2008
    2008
    Citations: 22
  • Polymorphisms in SIGLEC1 contribute to susceptibility to pulmonary active tuberculosis possibly through the modulation of IL-1ß.
    D Souza de Lima, VCL Nunes, MM Ogusku, A Sadahiro, A Pontillo, ...
    Infection, Genetics and Evolution 55, 313-317 , 2017
    2017
    Citations: 20