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Inflammatory bowel diseases (IBD), including Crohn's disease, ulcerative colitis, and unclassified inflammatory bowel disease, are a group of chronic, immune mediated conditions that are presumed to occur in genetically susceptible individuals because of a dysregulated intestinal immune response to environmental factors. IBD patients can be considered subjects with an aberrant immune response that makes them at increased risk of infections, particularly those due to opportunistic pathogens. In many cases this risk is significantly increased by the therapy they receive. Aim of this narrative review is to describe the impact of SARS-CoV-2 infection and the immunogenicity of COVID-19 vaccines in patients with IBD. Available data indicate that patients with IBD do not have an increased susceptibility to infection with SARS-CoV-2 and that, if infected, in the majority of the cases they must not modify the therapy in place because this does not negatively affect the COVID-19 course. Only corticosteroids should be reduced or suspended due to the risk of causing severe forms. Furthermore, COVID-19 seems to modify the course of IBD mainly due to the impact on intestinal disease of the psychological factors deriving from the measures implemented to deal with the pandemic. The data relating to the immune response induced by SARS-CoV-2 or by COVID-19 vaccines can be considered much less definitive. It seems certain that the immune response to disease and vaccines is not substantially different from that seen in healthy subjects, with the exception of patients treated with anti-tumor necrosis factor alone or in combination with other immunosuppressants who showed a reduced immune response. How much, however, this problem reduces induced protection is not known. Moreover, the impact of SARS-CoV-2 variants on IBD course and immune response to SARS-CoV-2 infection and COVID-19 vaccines has not been studied and deserves attention. Further studies capable of facing and solving unanswered questions are needed in order to adequately protect IBD patients from the risks associated with SARS-CoV-2 infection.
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http://dx.doi.org/10.3389/fimmu.2022.933774 | DOI Listing |
J Clin Invest
September 2025
Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Boston, United States of America.
B-lymphocytes play major adaptive immune roles, producing antibody and driving T-cell responses. However, how immunometabolism networks support B-cell activation and differentiation in response to distinct receptor stimuli remains incompletely understood. To gain insights, we systematically investigated acute primary human B-cell transcriptional, translational and metabolomic responses to B-cell receptor (BCR), Toll-like receptor 9 (TLR9), CD40-ligand (CD40L), interleukin-4 (IL4) or combinations thereof.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Centre for Experimental Medicine & Rheumatology, William Harvey Research Institute and Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
MS4A4A belongs to the MS4A tetraspan protein superfamily and is selectively expressed by the monocyte-macrophage lineage. In this study, we aimed to evaluate the role of MS4A4A+ macrophages in rheumatoid arthritis (RA) pathogenesis and response to treatment. RNA sequencing and immunohistochemistry of synovial samples from either early treatment-naïve or active chronic RA patients showed that MS4A4A expression positively correlated with synovial inflammation.
View Article and Find Full Text PDFInfect Immun
September 2025
Institute of Medical Microbiology and Hospital Hygiene, Heinrich Heine University, Düsseldorf, Germany.
Lymphotoxin β receptor (LTβR/TNFRSF3) signaling plays a crucial role in immune defense. Notably, LTβR-deficient (LTβR) mice exhibit severe defects in innate and adaptive immunity against various pathogens and succumb to infection. Here, we investigated the bone marrow (BM) and peritoneal cavity (PerC) compartments of LTβR mice during infection, demonstrating perturbed B-cell and T-cell subpopulations in the absence of LTβR signaling.
View Article and Find Full Text PDFInfect Immun
September 2025
School of Veterinary Medicine and Biomedical Sciences, University of Nebraska, Lincoln, Nebraska, USA.
Cell death mechanisms play a fundamental role in mycobacterial pathogenesis. We critically reviewed 94 research manuscripts, 44 review articles, and 4 book chapters to analyze important discoveries, background literature, and potential shortcomings in the field. The focus of this review is the pathogen (Mtb) and other Mtb and complex microorganisms.
View Article and Find Full Text PDFInfect Immun
September 2025
National Contagious Bovine Pleuropneumonia Reference Laboratory, State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China.
Contagious bovine pleuropneumonia (CBPP), caused by subsp. (Mmm), is a devastating cattle disease with high morbidity and mortality, threatening cattle productivity in Sub-Saharan Africa and potentially in parts of Asia. Cross-border livestock trade increases the risk of CBPP introduction or reintroduction.
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