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A deeper understanding of the immunological events during pregnancy will provide novel insights into the pathogenesis of pregnancy complications. The fundamental function of T follicular helper (Tfh) cells is to provide cognate help to B cells. Dysregulations of Tfh-cell function and/or development can result in various immunological diseases. However, the role and characteristics of Tfh cells during pregnancy remain unknown. Herein, an allogeneic-normal-pregnant mouse model was used, and we found that the CD4 T cells residing at the uterus and placenta (UP) displayed a Tfh-like phenotype; and the UP-derived CD4CXCR5PD-1 and CD4CXCR5ICOS Tfh cells, which showed a memory/activation phenotype, reached their peak at mid-pregnancy. These Tfh cells were located abundantly in the uterus at mid-pregnancy, but greatly increased in the placenta at late-pregnancy. Furthermore, increased foetal resorption by PDL1 blockade correlated with enhanced accumulation of Tfh cells and upregulated expressions of ICOS and PD-1 on these cells. Collectively, our findings are the first to indicate that an adequate and balanced accumulation of Tfh cells during gestation is likely to help maintaining a successful pregnancy, whereas an excessively high level of these cells could lead to abortion.
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http://dx.doi.org/10.1038/srep36560 | DOI Listing |
Nat Immunol
September 2025
Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
CD4 T follicular helper (T) cells support tailored B cell responses against multiple classes of pathogens. To reveal how diverse T phenotypes are established, we profiled mouse T cells in response to viral, helminth and bacterial infection. We identified a core T signature that is distinct from CD4 T follicular regulatory and effector cells and identified pathogen-specific transcriptional modules that shape T function.
View Article and Find Full Text PDFJ Immunol
September 2025
Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Qidong-Fudan Innovative Institution of Medical Sciences, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large quantities of subviral particles containing its surface antigen (HBsAg). T cells play a central role in controlling HBV infection but can also mediate liver injury and contribute to disease progression. However, the mechanisms that regulate T-cell responses to eliminate the virus without causing immunopathology during acute HBV infection remain poorly defined.
View Article and Find Full Text PDFJCI Insight
September 2025
Institute of Pathology, Department of Laboratory Medicine and Pathology, Lausanne University Hospital and Lausanne University, Lausanne, Switzerland.
The regulation of follicular (F) and germinal center (GC) immune reactivity in human lymph nodes (LNs), particularly during the acute stages of viral infection, remains poorly understood: We have analyzed lung-draining lymph nodes (LD-LNs) from COVID-19 autopsies using multiplex imaging and spatial transcriptomics to examine the immune landscape with respect to follicular immune reactivity. We identified three groups of donors based on the Bcl6 prevalence of their Reactive Follicles (RFs): RF-Bcl6no/low, RF-Bcl6int, and RF-Bcl6high. A distinct B/TFH immune landscape, associated with increased prevalence of proliferating B-cell and TFH-cell subsets, was found in RF-Bcl6high LD-LNs.
View Article and Find Full Text PDFBackground: The lncRNA-miRNA-mRNA regulatory network is recognized for its significant role in cardiovascular diseases, yet its involvement in in-stent restenosis (ISR) remains unexplored. Our study aimed to investigate how this regulatory network influences ISR occurrence and development by modulating inflammation and immunity.
Methods: By utilizing data extracted from the Gene Expression Omnibus (GEO) database, we constructed the lncRNA-miRNA-mRNA regulatory network specific to ISR.
Front Neurol
August 2025
Department of Neurology, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, China.
Background: Myasthenia gravis (MG), an autoimmune disorder characterized by B cell-driven autoantibody production, exhibits heterogeneous B cell subsets dysregulation and incompletely defined signaling mechanisms.
Methods: A cohort of 20 naïve MG patients positive for anti-acetylcholine receptor (AChR) antibodies and 15 healthy controls was analyzed. Peripheral blood mononuclear cells underwent proteomic profiling, flow cytometry (age-associated B cells (ABCs), plasma cells, T follicular helper cells, and regulatory B cells), and western blot validation of nuclear factor kappa-B (NF-κB)/cellular reticuloendotheliosis oncogene homolog (c-Rel) expression.