Carla Claser

ORCID: 0000-0002-5395-9632
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About
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Research Areas
  • Malaria Research and Control
  • Mosquito-borne diseases and control
  • Trypanosoma species research and implications
  • Research on Leishmaniasis Studies
  • Complement system in diseases
  • Immune Cell Function and Interaction
  • Viral Infections and Vectors
  • Parasitic Infections and Diagnostics
  • Parasites and Host Interactions
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immune cells in cancer
  • Toxoplasma gondii Research Studies
  • Autoimmune and Inflammatory Disorders Research
  • Immune Response and Inflammation
  • T-cell and B-cell Immunology
  • interferon and immune responses
  • Immunotherapy and Immune Responses
  • T-cell and Retrovirus Studies
  • Vector-Borne Animal Diseases
  • Vector-borne infectious diseases
  • Computational Drug Discovery Methods
  • Mast cells and histamine
  • Viral Infections and Outbreaks Research
  • Drug Transport and Resistance Mechanisms
  • Lanthanide and Transition Metal Complexes

Universidade Federal de São Paulo
2004-2024

Universidade de São Paulo
2021-2024

Singapore Immunology Network
2012-2024

Agency for Science, Technology and Research
2012-2024

Abstract Chikungunya virus (CHIKV) is an alphavirus that causes chronic and incapacitating arthralgia in humans. Injury to the joint believed occur because of viral host immune-mediated effects. However, exact involvement different immune mediators CHIKV-induced pathogenesis unknown. In this study, we assessed roles T cells primary CHIKV infection, replication dissemination, persistence, as well mediation disease severity adult RAG2−/−, CD4−/−, CD8−/−, wild-type C57BL/6J mice depleted CD4+...

10.4049/jimmunol.1202177 article EN The Journal of Immunology 2012-12-04

Microscopic examination of Giemsa-stained thin blood smears remains the gold standard method used to quantify and stage malaria parasites. However, this technique is tedious requires trained microscopists. We have developed a fast simple flow cytometry stage, various parasites in red cells whole or vitro cultured Plasmodium falciparum. The were stained with dihydroethidium Hoechst 33342 SYBR Green I leukocytes identified an antibody against CD45. Depending on DNA stains used, samples...

10.1038/srep00118 article EN cc-by-nc-sa Scientific Reports 2011-10-14

Background Infection with Plasmodium berghei ANKA (PbA) in susceptible mice induces a syndrome called experimental cerebral malaria (ECM) severe pathologies occurring various mouse organs. Immune mediators such as T cells or cytokines have been implicated the pathogenesis of ECM. Red blood infected PbA parasites shown to accumulate brain and other tissues during infection. This accumulation is thought be involved PbA–induced pathologies, which mechanisms are poorly understood. Methods...

10.1371/journal.pone.0018720 article EN cc-by PLoS ONE 2011-04-11

Abstract Cerebral malaria is a devastating complication of Plasmodium falciparum infection. Its pathogenesis complex, involving both parasite‐ and immune‐mediated events. CD8 + T cells play an effector role in murine experimental cerebral (ECM) induced by berghei ANKA (PbA) We have identified highly immunogenic epitope glideosome‐associated protein 50 that conserved across rodent species. Epitope‐specific are during PbA infection, migrating to the brain just before neurological signs...

10.1002/emmm.201202273 article EN cc-by EMBO Molecular Medicine 2013-05-16

The balance between pro-inflammatory and regulatory immune responses in determining optimal T cell activation is vital for the successful resolution of microbial infections. This maintained part by negative regulators activation, CTLA-4 PD-1/PD-L, which dampen effector during chronic However, their role acute infections, such as malaria, remains less clear. In this study, we determined contribution PD-1/PD-L to regulation Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria...

10.1371/journal.ppat.1002504 article EN cc-by PLoS Pathogens 2012-02-02

Abstract Plasmodium infections trigger strong innate and acquired immune responses, which can lead to severe complications, including the most feared often fatal cerebral malaria (CM). To begin dissect roles of different dendritic cell (DC) subsets in Plasmodium-induced pathology, we have generated a transgenic strain, Clec9A-diphtheria toxin receptor that allows us ablate vivo Clec9A+ DCs. Specifically, analyzed contribution this DC subset an experimental CM model using berghei, provide...

10.4049/jimmunol.1201171 article EN The Journal of Immunology 2012-06-26

Malaria-associated acute respiratory distress syndrome (ARDS) and lung injury (ALI) are life-threatening manifestations of severe malaria infections. The pathogenic mechanisms that lead to complications, such as vascular leakage, remain unclear. Here, we confirm depleting CD8+T cells with anti-CD8β antibodies in C57BL/6 mice infected P. berghei ANKA (PbA) prevent pulmonary leakage. When transfer activated parasite-specific into PbA-infected TCRβ-/- (devoid all T-cell populations), leakage...

10.1038/s41467-019-12017-8 article EN cc-by Nature Communications 2019-09-18

Protection against protozoan parasite Trypanosoma cruzi has been shown to be dependent on the induction of type 1 immune responses. Replication-deficient human 5 recombinant adenoviruses have an unsurpassed ability induce Thus, we constructed two encoding antigens trans-sialidase (rAdTS) and amastigote surface protein-2 (rAdASP2). Both were genetically engineered secrete products in order both optimal antibody T cell Immunizations mice with rAdASP2 rAdTS induced high levels serum antibodies...

10.1089/hum.2006.17.898 article EN Human Gene Therapy 2006-09-01

Abstract Interference or competition between CD8+ T cells restricted by distinct MHC-I molecules can be a powerful means to establish an immunodominant response. However, its importance during infections is still questionable. In this study, we describe that following infection of mice with the human pathogen Trypanosoma cruzi, cell immune response developed directed H-2Kb-restricted epitope expressed members trans-sialidase family surface proteins. To determine whether immunodominance was...

10.4049/jimmunol.180.3.1737 article EN The Journal of Immunology 2008-02-01

Protective immunity against lethal infection is developed when BALB/c or C57BL/6 mice are immunized with plasmids containing genes from the protozoan parasite Trypanosoma cruzi. However, genetic vaccination of highly susceptible mouse strain A/Sn promoted limited survival after challenge. This observation questioned whether this type would be appropriate for individuals. Here, we compared protective efficacy and immune response individual combined encoding trans-sialidase (TS) amastigote...

10.1089/hum.2004.15.878 article EN Human Gene Therapy 2004-09-01

Nucleoside hydrolases (NHs) show homology among parasite protozoa, fungi and bacteria. They are vital protagonists in the establishment of early infection and, therefore, excellent candidates for pathogen recognition by adaptive immune responses. Immune protection against NHs would prevent disease at several pathogens. We have identified domain NH L. donovani (NH36) responsible its immunogenicity protective efficacy murine visceral leishmaniasis (VL). Using recombinant generated peptides...

10.1371/journal.pntd.0000866 article EN cc-by PLoS neglected tropical diseases 2010-11-09

Immunisation with Amastigote Surface Protein 2 (asp-2) and trans-sialidase (ts) genes induces protective immunity in highly susceptible A/Sn mice, against infection parasites of the Y strain Trypanosoma cruzi. Based on immunological biological variations T. cruzi parasites, our goal was to validate vaccination results using different parasite strains. Due importance CD8+ T cells immunity, we initially determined which strains expressed immunodominant H-2Kk-restricted epitope TEWETGQI. We...

10.1016/j.vaccine.2009.07.013 article EN publisher-specific-oa Vaccine 2009-07-26

Abstract Co-infection with Plasmodium and chikungunya virus (CHIKV) has been reported in humans, but the impact of co-infection on pathogenesis remains unclear. Here, we show that prior exposure to suppresses CHIKV-associated pathologies mice. Mechanistically, infection induces IFNγ, which reduces viraemia a subsequent CHIKV tissue viral load joint inflammation. Conversely, concomitant both pathogens limits peak inflammation no effect viraemia. Reduced is regulated by elevated apoptosis CD4...

10.1038/s41467-018-06227-9 article EN cc-by Nature Communications 2018-09-19

Research Article7 November 2017Open Access Transparent process Co-infection with Chikungunya virus alters trafficking of pathogenic CD8+ T cells into the brain and prevents Plasmodium-induced neuropathology Teck-Hui Teo Singapore Immunology Network, Agency for Science, Technology (A*STAR), Singapore, Search more papers by this author Shanshan W Howland Carla Claser Sin Yee Gun Chek Meng Poh Wendy WL Lee Fok-Moon Lum orcid.org/0000-0002-5645-7048 Lisa FP Ng Corresponding Author [email...

10.15252/emmm.201707885 article EN cc-by EMBO Molecular Medicine 2017-11-07

Type I IFN signaling suppresses splenic T helper 1 (Th1) responses during blood-stage Plasmodium berghei ANKA (PbA) infection in mice, and is crucial for mediating tissue accumulation of parasites fatal cerebral symptoms via mechanisms that remain to be fully characterized. Interferon regulatory factor 7 (IRF7) considered a master regulator type responses. Here, we assessed IRF7 its roles lethal PbA nonlethal chabaudi AS (PcAS) as two distinct models malaria. We found was not essential...

10.1002/eji.201444824 article EN European Journal of Immunology 2014-10-16
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