Early exposure to immune stimuli, including maternal infection during the perinatal period, is increasingly recognized to affect immune predisposition during later life. This includes exposure to not only viral and bacterial infection but also parasitic helminths which remain widespread. Noted effects of helminth infection, including altered incidence of atopic inflammation and vaccine responsiveness, support further research into the impact these infections have for skewing immune responses. At the same time, despite a sea of recommendations, clear phenotypic and mechanistic understandings of how environmental perturbations in pregnancy and nursing modify immune predisposition and allergy in offspring remain unrefined. Schistosomes, as strong inducers of type 2 immunity embedded in a rich network of regulatory processes, possess strong abilities to shift inflammatory and allergic diseases in infected hosts, for example by generating feedback loops that impair T cell responses to heterologous antigens. Based on the current literature on schistosomiasis, we explore in this review how maternal schistosome infection could drive changes in immune system development of offspring and how this may lead to identifying factors involved in altering responses to vaccination as well as manifestations of immune disorders including allergy.
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http://dx.doi.org/10.3389/fimmu.2018.02960 | DOI Listing |
Sci Rep
January 2025
USDA, Agricultural Research Service, US National Poultry Research Center, 934 College Station Road, Athens, GA, 30605, USA.
Marek's disease (MD), a T cell lymphoma disease in chickens, is caused by the Marek's disease virus (MDV) found ubiquitously in the poultry industry. Genetically resistant Line 6 (L6) and susceptible Line 7 (L7) chickens have been instrumental to research on avian immune system response to MDV infection. In this study we characterized molecular signatures unique to splenic immune cell types across different genetic backgrounds 6 days after infection.
View Article and Find Full Text PDFNeurobiol Dis
January 2025
Departments of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA. Electronic address:
The adenosine triphosphate-binding cassette transporter A7 (ABCA7) gene is ranked as one of the top susceptibility loci for Alzheimer's disease (AD). While ABCA7 mediates lipid transport across cellular membranes, ABCA7 loss of function has been shown to exacerbate amyloid-β (Aβ) pathology and compromise microglial function. Our family-based study uncovered an extremely rare ABCA7 p.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
January 2025
The University of Texas Medical Branch at Galveston, Microbiology and Immuology, Galveston, Texas, United States.
Exposure to influenza A virus (IAV), respiratory syncytial virus (RSV), and human metapneumovirus (hMPV) is well-known to increase the risk of pneumonia in humans. Type I interferon (IFN-I) is a hallmark response to acute viral infections, and alveolar macrophages (AMs) constitute the first line of airway defense against opportunistic bacteria. Our study reveals that virus-induced IFN-I receptor (IFNAR1) signaling directly impairs AM-dependent antibacterial protection.
View Article and Find Full Text PDFRheumatology (Oxford)
January 2025
Department of Cell Biology and Immunology, Institute of Parasitology and Biomedicine López-Neyra, CSIC, Granada, Spain.
Objectives: COVID-19 and systemic sclerosis (SSc) share multiple similarities in their clinical manifestations, alterations in immune response, and therapeutic options. These resemblances have also been identified in other immune-mediated inflammatory diseases where a common genetic component has been found. Thus, we decided to evaluate for the first time this shared genetic architecture with SSc.
View Article and Find Full Text PDFBurns
January 2025
Dermatology Hospital, Southern Medical University, Guangzhou, China. Electronic address:
Background: Keloid is a benign skin tumor that result from abnormal wound healing and excessive collagen deposition. The pathogenesis is believed to be linked to genetic predisposition and immune imbalance, although the precise mechanisms remain poorly understood. Current therapeutic approaches may not consistently yield satisfactory outcomes and are often accompanied by potential side effects and risks.
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