Paula Ferreira is member of the Immunobiology group at i3S-Instituto de Investigação e Inovação em Saúde, Director of the Laboratory of Immunology Mário Arala-Chaves and Professor of Immunology at higher school ICBAS-Instituto de Ciências Biomédicas Abel Salazar, Porto University. She has had an abiding interest in understanding the mechanisms by which the pathogen Group B Streptococcus (GBS) interact with the host immune system to succeed in their colonization. Her research work ultimately aims at the development of immune protective and/or therapeutic approaches against GBS-induced neonatal diseases (sepsis, pneumonia and meningitis). Research carried out by her team show that GBS utilizes its glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to evade the host immune system (J Immunol. 2007; 1;178(3):1379; Microbes and Infection. 2007; 9; 11: 1276; PLoS One. 2013 May 2;8(5):e63244). They showed that GBS GAPDH induces host IL-10 production promptly after GBS infection preventing the development of a protective immune response since this immunosuppressive cytokine impairs neutrophil recruitment (J Immunol. 2013; 191 (9): 4759), a host effector cell crucial for bacterial clearance, allowing bacterial colonization and survival within the host. Indeed, it is well known that the absence of neutrophil recruitment into infected organs is associated with newborn susceptibility to GBS infection. Therefore, they thought GBS GAPDH as a promising vaccine candidate against GBS (PLoS Pathog.2011 7(11):e1002363; PLoS One. 2012; 7(1): e29963). The absence of an animal model reproducing the natural infectious process limited the understanding of the disease and the development of effective treatments. Therefore, her research team developed a mouse model in which bacteria are transmitted to the offspring from vaginally colonised pregnant females, the natural route of infection (Nat Commun. 2018 Aug 7;9(1):3138). This new mouse model, that reproduces key steps of GBS infection in newborns, will promote a better understanding of the physiopathology of GBS-induced diseases and was used to test the GBS GAPDH vaccine. Since GAPDH is highly conserved, they verified that maternal vaccination interferes with the intestinal colonization of the offspring causing early-life gut dysbiosis, shapes intestinal mucosa and leads to altered behaviour and higher sensitivity to stress in their offspring during adulthood (Brain Behav Immun. 2022; 103:186), highlighting the danger of using ubiquitous antigens in maternal human vaccines against neonatal pathogens. P. Ferreira and collaborators in a Personal View (Lancet Infect Dis. 2021; 21(7):e191) argue that the prescription of fewer antibiotics and shorter treatment duration is just as effective as longer regimens and that shorter antibiotic treatments exert less selective pressure on microorganisms, preventing the development of resistance within commensal organisms. New therapeutic approaches beyond antibacterial treatment to control the outcome of neonatal sepsis are mandatory and adenosine triphosphate signalling is gaining more attention in the research field of systemic inflammation/infection and neuroinflammation. Tissue damage and inflammation lead to an increase in the systemic extracellular concentration of ATP, which is detected by P2 purinergic receptors (P2R). The main immunoregulator of P2R is the P2X7 receptor (P2X7R) which is expressed on innate and adaptive immune cells. In parallel, P2X7R was identified as a key player in the neuroinflammatory cascade, controlling the onset of progression of a wide range of neurological conditions and the pathophysiological processes involved in sepsis. P Ferreira joins Laura Oliveira's research team to address the therapeutic potential of P2X7R signalling in neonatal bacterial diseases. P. Ferreira is also interested in evaluating the impact of GBS neonatal infection on the development (evolution) of the immune system, joining to Pedro Ferreirinha's research.