Through my scientific career I have specialized in immunology. I have started my research path by working, during my master thesis, on antiapoptotic pathways and on their role as cell markers for peripheral differentiation and activation of ¿d T-cells, a sub-population of T-cells (Bruno Silva-Santos Lab iMM, Lisboa - DeBarros et al., Eur J Immunol, 2011; Ribot et al., J Immunol 2010). I have then pursued my doctoral studies on cell cycle and its influence in the early haematopoietic stages, namely the influence of cyclin D, that bridges the outer cellular milieu with the cell decision to cycle. We discovered that cyclin D1 had a non-canonical (cell cycle independent) regulatory effect which was essential for haematopoiesis, migration and proliferation in a stage that preceded T or B cell lineages. We also attributed this effect to exons 4 and 5 of the protein. The phenotype observed is dependent of the mouse development stage, being more severe until day 6 of development (Benedita Rocha Lab Necker, Paris - Chaves-Ferreira et al., Biol Direct, 2016). Later as a post doc I have bridged immunology with chemistry by studying the effect of carbon monoxide releasing molecules (CORM) effects on cancer cells and on peripheral blood mononuclear cells. By conjugating these ruthenium-based molecules to proteins we were able to target specifically tumour cells in the mouse host and regulate the expression of important pro inflammatory cytokines, involved on tumour metastization, through a positive feedback loop of Hif1a overexpression. The anti-inflammatory effect does not occur on white blood cells were this positive feedback loop is not triggered, making it perfect for in vivo use (GBernardes Lab iMM, Lisboa – Seixas and Chaves-Ferreira et al., Chemistry, 2015; Albuquerque et al., Chem Commun, 2015; Chaves-Ferreira et al., Angew Chem Int Ed Engl, 2015). I have then pursued bridging immunology with other research fields, this time, with parasitology and Glycobiology. I have studied glycosylation on T. brucei. We have developed tools to control the glycosylation of these proteins and found that expressing the conventional triantennary Man9GlcNAc2 or the T. brucei specific biantennary Man5GlcNAc2 or a mixture of both dolichol-linked oligosaccharide precursors affects the host distribution following infection, revealing yet another immune evasion characteristic of this parasite (LFigueiredo Lab iMM, Lisboa – Bevan et al European J. Org. Chem, 2018 and unpublished data). Afterwards, I joined Miguel Seabra Lab on CEDOC where I studied the mechanisms of cells death on Choroideremia (CHM), a rare congenital genetic eye disease. We produced a CHM disease model in ARPE-19 cells using CRISPR and described that these cells showed induced cell death via necroptosis, a cell death pathway modulated by TNF receptors. CHM mutation induced the expression of the MHC class 2 antigen in these cells, particularly upon IFN gamma stimulation. A finding that has clinical relevance which may suggest some degree of autoimmunity and bridges findings that had been reported in ex-vivo ocular analysis. (MSeabra Lab CEDOC, Lisboa, unpublished data). Changing gears from fundamental biology onto applied biotechnology, I joined in September 2020 – present, the lab of Vasco Barreto to develop CRISPR genetic engineering of long inserts on his support platform CRISPR@CEDOC. There I have developed extensive CRISPR hands on experience (VBarreto Lab CEDOC, Lisboa – Vicente et al. Front. Cell Dev. Biol, 2021) as well as molecular biology knowledge and developed several challenging techniques and protocols to further increase the efficiency of long insertions. I have also improved my cell culture techniques with IPS cells. Joining a highly technical service platform of gene engineering has given me a purpose of developing science for direct application that I have very much appreciated and am committed in further developing.