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Juliana soarez

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There are cases of data loss that are really serious and that can compromise the continuity of a business or an […]. To cover the multiple facets of human disease we have established an interdisciplinary approach combining: clinical, bioinformatics, cellular and molecular immunology and cutting-edge microscopy.

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Plasticity endows T cells to be influenced by their microenvironment and respond to it accordingly. A specific microenvironment is defined by a variety of factors, including biological and chemical composition, cell-cell interactions, but also metabolic and mechanical cues.

CD4 T cells are key drivers of rheumatoid arthritis RA , the most common inflammatory rheumatic disease. There is an unmet need for therapies that precisely target the mechanisms underpinning CD4 T cell dysregulation rather than overall T cell activation or the end products, inflammatory cytokines.

In rheumatoid arthritis, elucidating how the joint microenvironment imprints dysregulated T cell inflammation, drives and possibly diversifies their pathological functions could broaden the potential therapeutic targets, extending beyond the successful blockade of end-stage inflammatory mediators.

Our research breaches immunology and clinical studies. We start with clinical data and tissue samples from patients and probe for the cellular and molecular mechanisms involved.

This research line focuses on defining the basis and consequences of pathogenic T cell populations in the development of Rheumatoid Arthritis.

Additionally, tissue explants will be used to elucidate the role of tissue microenvironment in driving joint chronic inflammation. The compounded contribution of host intrinsic factors, immunological niches and viral genetic diversity to HIV-1 pathogenesis remain largely unknown.

First, sex has been a neglected host intrinsic variable, yet women display faster HIV disease progression. Second, the immunological niche offered by follicular T Tfh cells allows for HIV-1 ongoing replication even in successfully treated patients.

Finally, most of current knowledge on HIV-1 pathogenicity is based on the study of the fairly infrequent subtype B. The mechanisms underlying HIV-female bias, the establishment of Tfh replicating reservoirs and how HIV-genetic diversity impinge on pathogenicity remain largely undefined.

We are addressing HIV-1 infection as a continuum of host intrinsic biological factors, immunological niches and HIV-1 genetic diversity.

HIV-1 is primarily an infection of lymphoid tissues. Anti-retroviral therapy ART has rendered HIV-1 infection a manageable illness for those with access to treatment, still it does not clear reservoirs where the virus persists.

To dissect cellular and molecular characteristics of the follicular reservoir we are using human follicular T cells isolated from human tonsils through fluorescence-activated cell sorting FACS and infect them ex vivo with HIV We are pursuing the identification, at the molecular level, the activation and metabolic pathways hijacked by HIV-1 through a combination of flow cytometry, metabolic assays and confocal analysis.

Women mount stronger immune responses and experience more severe HIV-1 pathogenesis. The precise mechanism mediating the sexual dimorphism in HIV-1 pathogenesis is not known, partly because sex has not been considered a biological variable.

Using human blood and tonsillar samples, we aim at identifying the molecular determinants underpinning the interplay between sex hormones and HIV-1 infection in order to identify potential pathways for intervention, and to rationally control for biological differences relevant to therapeutic efficacy outcomes.

However, distinct HIV-1 subtypes have different biological properties including disease progression rates and cellular tropism.

The impact of HIV genetic diversity can only be optimally undertaken in countries with high HIV genetic diversity through first-rate clinical registry.

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