Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1365-2516.2008.01965.xDOI Listing

Publication Analysis

Top Keywords

immune tolerance
4
tolerance induction
4
induction high
4
high von
4
von willebrand
4
willebrand factor/factor
4
factor/factor viii
4
viii content
4
content ratio
4
ratio concentrate
4

Similar Publications

Antiviral therapy for hepatitis B virus infection is beneficial for the prognosis hepatocellular carcinoma.

World J Gastrointest Oncol

January 2025

Institute of Liver Diseases, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun 130061, Jilin Province, China.

In this editorial, we comment on the article by Mu , published in the recent issue of the . We pay special attention to the immune tolerance mechanism caused by hepatitis B virus (HBV) infection, the pathogenesis of hepatocellular carcinoma (HCC), and the role of antiviral therapy in treating HCC related to HBV infection. HBV infection leads to systemic innate immune tolerance by directly inhibiting pattern recognition receptor recognition and antiviral signaling pathways, as well as by inhibiting the immune functions of macrophages, natural killer cells and dendritic cells.

View Article and Find Full Text PDF

Parasitic helminths secrete extracellular vesicles (EVs) into their host tissues to modulate immune responses, but the underlying mechanisms are poorly understood. We demonstrate that Ascaris EVs are efficiently internalised by monocytes in human peripheral blood mononuclear cells and increase the percentage of classical monocytes. Furthermore, EV treatment of monocytes induced a novel anti-inflammatory phenotype characterised by CD14, CD16, CC chemokine receptor 2 (CCR2) and programmed death-ligand 1 (PD-L1) cells.

View Article and Find Full Text PDF

Biometallic ions and derivatives: a new direction for cancer immunotherapy.

Mol Cancer

January 2025

Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 41001l, China.

Biometallic ions play a crucial role in regulating the immune system. In recent years, cancer immunotherapy has become a breakthrough in cancer treatment, achieving good efficacy in a wide range of cancers with its specificity and durability advantages. However, existing therapies still face challenges, such as immune tolerance and immune escape.

View Article and Find Full Text PDF

Signatures of H3K4me3 modification predict cancer immunotherapy response and identify a new immune checkpoint-SLAMF9.

Respir Res

January 2025

Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.

H3 lysine 4 trimethylation (H3K4me3) modification and related regulators extensively regulate various crucial transcriptional courses in health and disease. However, the regulatory relationship between H3K4me3 modification and anti-tumor immunity has not been fully elucidated. We identified 72 independent prognostic genes of lung adenocarcinoma (LUAD) whose transcriptional expression were closely correlated with known 27 H3K4me3 regulators.

View Article and Find Full Text PDF

Newly identified cell types crucial for gut commensal tolerance.

Trends Cell Biol

January 2025

Department of Immunology, Ophthalmology, and ENT, Universidad Complutense de Madrid, Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), Madrid, Spain. Electronic address:

The generation of regulatory T cells (Tregs) through interactions with antigen-presenting cells (APCs) is essential for establishing tolerance to gut commensals. Recent findings highlight the critical role of RORγt-lineage APCs, especially in gut-associated lymphoid tissues, in the induction of microbiota-specific peripheral Tregs and maintaining gut immune homeostasis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!