ORCID Profile
0000-0003-4511-7918
Current Organisations
University of Buenos Aires
,
Walter and Eliza Hall Institute of Medical Research
,
Oak Ridge National Laboratory
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Publisher: Elsevier BV
Date: 06-2022
Publisher: EMBO
Date: 04-2022
Publisher: Cold Spring Harbor Laboratory
Date: 05-05-2020
DOI: 10.1101/2020.05.05.078717
Abstract: γδ T cells play an essential role in the immune response to malaria infection. However, long-lasting effects of malaria infection on the γδ T cell population still remain inadequately understood. This study investigated transcriptional changes and memory-like functional capacity of malaria pre-exposed γδ T cells using a Plasmodium chabaudi infection model. We show that multiple genes associated with effector function (chemokines, cytokines and cytotoxicity) and antigen-presentation were upregulated in P. chabaudi -exposed γδ T cells compared to γδ T cells from naïve mice. This transcriptional profile was positively correlated with profiles observed in conventional memory CD8 + T cells and was accompanied by enhanced reactivation upon secondary encounter with Plasmodium -infected red blood cells in vitro . Collectively our data demonstrate that Plasmodium exposure result in “memory-like imprints” in the γδ T cell population and also promotes γδ T cells that can support antigen-presentation during subsequent infections.
Publisher: Cambridge University Press (CUP)
Date: 13-12-2019
DOI: 10.1017/S0031182019001744
Abstract: The CXCR3 chemokine CXCL10 or IFN- γ inducible protein 10 (IP-10) has been identified as an important biomarker of cerebral malaria (CM) mortality in children. Studies in mouse malaria infection models have shown that CXCL10 blockade alleviates brain intravascular inflammation and protects infected mice from CM. Despite the key role that CXCL10 plays in the development of CM, the leucocytic sources of CXCL10 in response to human malaria are not known. Here we investigated CXCL10 responses to Plasmodium falciparum in peripheral blood mononuclear cells (PBMCs). We found that PBMCs from malaria-unexposed donors produce CXCL10 in response to P. falciparum and that this response is IFN- γ -dependent. Moreover, CD14 + monocytes were identified as the main leucocytic sources of CXCL10 in peripheral blood, suggesting an important role for innate immune responses in the activation of this pathway involved in the development of symptomatic malaria.
Publisher: Elsevier BV
Date: 2014
Publisher: Springer Science and Business Media LLC
Date: 13-04-2023
DOI: 10.1186/S12929-023-00916-4
Abstract: Typical symptoms of uncomplicated dengue fever (DF) include headache, muscle pains, rash, cough, and vomiting. A proportion of cases progress to severe dengue hemorrhagic fever (DHF), associated with increased vascular permeability, thrombocytopenia, and hemorrhages. Progression to severe dengue is difficult to diagnose at the onset of fever, which complicates patient triage, posing a socio-economic burden on health systems. To identify parameters associated with protection and susceptibility to DHF, we pursued a systems immunology approach integrating plasma chemokine profiling, high-dimensional mass cytometry and peripheral blood mononuclear cell (PBMC) transcriptomic analysis at the onset of fever in a prospective study conducted in Indonesia. After a secondary infection, progression to uncomplicated dengue featured transcriptional profiles associated with increased cell proliferation and metabolism, and an expansion of ICOS + CD4 + and CD8 + effector memory T cells. These responses were virtually absent in cases progressing to severe DHF, that instead mounted an innate-like response, characterised by inflammatory transcriptional profiles, high circulating levels of inflammatory chemokines and with high frequencies of CD4 low non-classical monocytes predicting increased odds of severe disease. Our results suggests that effector memory T cell activation might play an important role ameliorating severe disease symptoms during a secondary dengue infection, and in the absence of that response, a strong innate inflammatory response is required to control viral replication. Our research also identified discrete cell populations predicting increased odds of severe disease, with potential diagnostic value.
Publisher: Cambridge University Press (CUP)
Date: 13-04-2020
DOI: 10.1017/S003118202000061X
Abstract: Emerging evidence started to delineate multiple layers of memory B cells, with distinct effector functions during recall responses. Whereas most studies examining long-lived memory B cell responses have focussed on the IgG + memory B cell compartment, IgM + memory B cells have only recently started to receive attention. It has been proposed that unlike IgG + memory B cells, which differentiate into antibody-secreting plasma cells upon antigen re-encounter, IgM + memory B cells might have the additional capacity to establish secondary germinal centre (GC) responses. The precise function of IgM + memory B cells in the humoral immune response to malaria has not been fully defined. Using a murine model of severe malaria infection and adoptive transfer strategies we found that IgM + memory B cells induced in responses to P. berghei ANKA readily proliferate upon re-infection and adopt a GC B cell-like phenotype. The results suggest that that IgM + memory B cells might play an important role in populating secondary GCs after re-infection with Plasmodium, thereby initiating the induction of B cell clones with enhanced affinity for antigen, at faster rates than naive B cells.
Location: Australia
No related grants have been discovered for Diana Hansen.