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Introduction: Children's rapid development and immature immune systems place them at a higher risk of adverse health outcomes associated with air pollution exposure. However, the specific mechanisms in which air pollution mediates immune dysregulation in youth are poorly understood. Thus, we aimed to systematically review the available epidemiological evidence surrounding the effects of indoor and ambient air pollution exposure on systemic immune biomarkers in early life (from birth to 18 years old)., Methods: based on PRISMA guidelines, we developed a systematic search strategy and defined inclusion and exclusion criteria to retrieve publications from PubMed, SCOPUS and Web of Science published up to August 10th, 2024. Quality assessment and evidence evaluation were also performed. Five independent reviewers participated in the process., Results: In total, 96 studies were included. We found limited evidence of a causal relationship between prenatal ambient PM 2.5 and reduced T-cells (CD3 + and CD8 + ), as well as between postnatal PM exposure and increased IgE levels or allergic sensitization. For the rest of exposure-outcome combinations we classified the evidence as inadequate, mainly due to the limited number of studies available or the lack of consistency in the results obtained among them. This was particularly the case for indoor air pollution research, for which only 12 studies were available., Conclusion: the present systematic review highlights the need for further research on the impacts of air pollution on youth's immune system. We provided recommendations for future studies in order to better understand the early subclinical and clinical effects of air pollution and the underlying biological pathways, and identify the dynamics of the innate and adaptive immune responses to environmental threats. Considering the significance of childhood immunity on health outcomes within all stages of life, and the globally extensive burden of air pollution exposure, further research on this topic should be prioritized., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Mireia Gascon reports financial support was provided by Carlos III Health InstituteHealth Sciences National Library. Gemma Moncunill reports financial support was provided by the Agencia Estatal de Investigación (AEI; State Research Agency) of the Spanish Government. Yana Luo reports support from China Scholarship Council (202308620109). If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 Elsevier Inc. All rights reserved.)

Background: The RTS,S/AS01 E malaria vaccine showed lower antibody response and protective efficacy in infants aged 6-12 weeks compared with children aged 5-17 months (for whom this vaccine is recommended). We aimed to study the effect of previous Plasmodium falciparum exposure on the antibody responses to RTS,S/AS01 E vaccination in infants and children, and the mediating effect of baseline (including maternal) anti-circumsporozoite protein (CSP) antibodies., Methods: In this observational study, we included children and infants from six African countries (Burkina Faso, Gabon, Ghana, Kenya, Mozambique, and Tanzania) enrolled in the MAL067 immunology ancillary study of the RTS,S/AS01 E phase 3 clinical trial from March 27, 2009, to Jan 21, 2011. We used comparator-vaccinated infants and children to identify antibody-based signatures of previous P falciparum exposure, which were later applied to RTS,S/AS01 E -vaccinated infants and children. In these participants, we explored the relationship between vaccine antibody immunoglobulin G (IgG) responses measured by ELISA and pre-vaccination serological markers of malaria exposure by assessing the IgG levels against 1000 P falciparum antigens using partial proteome microarrays., Findings: We included 718 comparator-vaccinated infants (348 [48%]) and children (370 [52%]) and 606 RTS,S/AS01 E -vaccinated infants (329 [54%]) and children (277 [46%]). Anti-CSP IgG responses to primary vaccination did not correlate with a baseline signature of previous exposure in children, suggesting that prior P falciparum exposure does not significantly affect antibody immunogenicity in children (Pearson's r=-0·02 [95% CI -0·13 to 0·10]). By contrast, high P falciparum exposure signature levels at the time of vaccination in infants, presumably driven by maternally transferred antibodies and declining within the initial 6-12 months of life, correlated with reduced RTS,S/AS01 E responses (r=-0·17 [-0·27 to -0·06]). This negative correlation was stronger for anti-CSP IgG than for the exposure signature or any other more immunogenic blood stage P falciparum antigens (r=-0·42 [-0·50 to -0·33]), persisted after adjustment by baseline levels of the exposure signature (semi-partial correlation r=-0·44 [-0·55 to -0·33]), and involved antibodies to the central NANP region (r=-0·39 [-0·49 to -0·28]) but not the C-terminal region (r=0·02 [-0·10 to 0·15]) of CSP. The negative effect of maternal anti-CSP IgG in infants did not appear to be confounded by other malaria transmission-dependent variables., Interpretation: Interference between passive immunity and vaccine response is clinically significant and might affect the implementation of next-generation CSP-based vaccines for young infants and mothers as well as passive immunisation with human monoclonal antibodies., Funding: US National Institutes of Health, National Institute of Allergy and Infectious Diseases; PATH-Malaria Vaccine Initiative; Spanish Ministerio de Economía y Competitividad (Instituto de Salud Carlos III), European Regional Development Fund and European Social Fund; Fundación Ramón Areces; Spanish Ministry of Science and Innovation; and Generalitat de Catalunya (CERCA Program)., Competing Interests: Declaration of interests JJC is an employee of Antigen Discovery, a company that carries patents (US Patent 10174311 and US Patent 20160320404) related to the protein microarray analyses used here and where the arrays were conducted. All other authors declare no competing interests., (Copyright © 2024 Elsevier Ltd. All rights reserved, including those for text and data mining, AI training, and similar technologies.)

Objectives: We aimed to evaluate the adaptive immune responses cross-recognition of the hypermutated SARS-CoV-2 BA.2.86 variant and identify the determinants influencing this recognition., Methods: We measured BA.2.86 neutralizing antibodies and T-cell responses cross-reactivity in previously exposed participants. We investigated clinical-demographic factors and used a novel in silico analysis to assess viral genetic determinants affecting T-cell responses., Results: Despite notable escape from neutralizing antibodies, T-cell responses remained generally preserved, albeit with a significant but small loss in T-cell cross-recognition (7.5%, 14.2%, and 10.8% average loss for IFN-γ, IL-2, and IFN-γ + IL-2, respectively, p<0.05). This is consistent with the prediction of 6 out of 10 immunodominant T-cell epitopes (TCEs) altered by BA.2.86 mutations to have reduced peptide presentation. This effect is expected to be mitigated by total TCEs across the genome. Remarkably, T-cell responses and cross-recognition were 3.5 (IFN-γ), 2 (IL-2) and 2.4 (IFN-γ + IL-2) times higher when first induced by infection rather than by vaccination three years earlier, by increasing number of infections, and by ancestral/Delta than Omicron infections., Conclusions: Our findings underscore the critical role and factors influencing T-cell immunity against evolving SARS-CoV-2 variants, such as first antigen encounter (vaccination or infection), as it is essential for developing effective control strategies., Competing Interests: Declaration of Competing Interest Unrelated to the present work JB received Institutional grants/agreements from/with MSD, HIPRA, GRIFOLS and NESAPOR; personal payments from HIPRA and NESAPOR; and was former CEO and founder of AlbaJuna Therapeutics, S.L. All other authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background Mental illnesses have been overlooked as a potential factor influencing antibody responses to COVID-19 vaccine. Associations between mental disorders and antibody response might vary by specific disorders, depend on the long-term course of the illness and relate to psychotropic treatment., Methods: The association between mental illness diagnoses (mood affective disorders, anxiety disorders, other) over ten years and psychotropic drug prescription based on electronic health records with antibody levels (IgG and IgA) post COVID-19 vaccination was assessed in 939 vaccinated adults from Catalonia, Spain. We employed linear regression models to assess associations between specific mental illnesses and psychotropic drugs with antibody levels, correcting for demographics, comorbidities and lifestyle factors. In a genotyped subset (n = 247) we assessed the effect of polygenic risk scores (PRS) for mental illnesses and performed a two-sample mendelian randomization (MR) analysis to examine causality between mental illness and antibody responses., Results: Mood affective disorders were associated with lower IgG to receptor binding domain (RBD) [percentage change = -26.37 (95 % CI, -42.00, -6.54)]. Diagnosis of anxiety disorders was not associated with the outcome. The group of other diagnoses (mainly including insomnia and nicotine dependence) were associated with lower IgG RBD levels [percentage change: -21.53 (95 % CI, -35.38, -4.71)] and recent onset cases (≤5 years ago) showed greater decline in antibody levels. Participants on second-generation antipsychotics and multiple classes of psychotropic drugs in the last 6 months exhibited lower antibody levels. In the genotyped population, higher genetic liability (higher PRS) to schizophrenia was associated with lower IgG RBD levels [percentage change = -35.49 (95 % CI, -56.55, -4.23)]. MR analysis revealed a causal relationship between major depression genetic instrumental variables and lower IgG RBD and S levels., Conclusions: These findings raise concerns about the efficacy of COVID-19 vaccines and potentially of other vaccines as well, in individuals with mood affective disorders, current/recent insomnia and nicotine dependence and people on multiple psychotropic drugs. Whether these associations are translated into increased risk for breakthrough infections and immune mediated long-term sequels of the SARS-CoV-2 infection warrants further investigation., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)