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TNFRSF6 induces mitochondrial dysfunction and microglia activation in the in vivo and in vitro models of sepsis-associated encephalopathy.
Cell Mol Biol (Noisy-le-grand)
March 2024
Department of Neurocritical Medicine, Taihe Hospital, Hubei University of Medicine, No. 32 Renmin South Road, Shiyan City 442000, Hubei Province, China.
Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis. The tumour necrosis factor receptor superfamily member 6 (TNFRSF6) gene encodes the Fas protein, and it participates in apoptosis induced in different cell types. This study aimed to explore TNFRSF6 function in SAE.
View Article and Find Full Text PDFPrimary immune regulatory disorders (PIRD): expanding the mutation spectrum in Turkey and identification of sixteen novel variants.
Immunol Res
August 2024
Department of Pediatric Health and Diseases, Department of Pediatric Immunology, Faculty of Medicine, Ege University, Izmir, Turkey.
Human Inborn Errors of Immunity (IEIs) encompass a clinically and genetically heterogeneous group of disorders, ranging from mild cases to severe, life-threatening types. Among these, Primary Immune Regulatory Disorders (PIRDs) constitute a subset of IEIs characterized by diverse clinical phenotypes, prominently featuring severe atopy, autoimmunity, lymphoproliferation, hyperinflammation, autoinflammation, and susceptibility to malignancies. According to the latest report from the International Union of Immunological Societies (IUIS), PIRDs arise from mutations in various genes including LYST, RAB27A, AP3B1, AP3D1, PRF1, UNC13D, STX11, STXBP2, FAAP24, SLC7A7, RASGRP1, CD70, CTPS1, RLTPR, ITK, MAGT1, PRKCD, TNFRSF9, SH2DIA, XIAP, CD27 (TNFRSF7), FAS (TNFRSF6), FASLG (TNFSF6), CASP10, CASP8, FADD, LRBA, STAT3, AIRE, ITCH, ZAP70, TPP2, JAK1, PEPD, FOXP3, IL2RA, CTLA4, BACH2, IL2RB, DEF6, FERMT1, IL10, IL10RA, IL10RB, NFAT5, TGFB1, and RIPK1 genes.
View Article and Find Full Text PDFNon-apoptotic FAS signaling controls mTOR activation and extrafollicular maturation in human B cells.
Sci Immunol
January 2024
Department of Rheumatology and Clinical Immunology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Article Synopsis
- Defective signaling of the FAS molecule, linked to autoimmune lymphoproliferative syndrome (ALPS), leads to hypergammaglobulinemia and fewer conventional memory B cells due to disrupted B cell differentiation.
- Analysis of ALPS patients revealed low memory B cell numbers, fewer germinal center B cells, and an expanded extrafollicular B cell response, indicating a shift in B cell fate.
- The study proposes that abnormal non-apoptotic FAS signaling affects the mTOR pathway and gene expression, contributing to the altered B cell responses observed in ALPS.
Combined germline and somatic human FADD mutations cause autoimmune lymphoproliferative syndrome.
J Allergy Clin Immunol
January 2024
University of Paris Cité, Paris, France; Laboratory of Immunogenetics of Pediatric Autoimmune Diseases, Imagine Institute, INSERM UMR 1163, Paris, France; Imagine Institute, INSERM UMR 1163, Paris, France. Electronic address:
Background: The autoimmune lymphoproliferative syndrome (ALPS) is a noninfectious and nonmalignant lymphoproliferative disease frequently associated with autoimmune cytopenia resulting from defective FAS signaling. We previously described germline monoallelic FAS (TNFRSF6) haploinsufficient mutations associated with somatic events, such as loss of heterozygosity on the second allele of FAS, as a cause of ALPS-FAS. These somatic events were identified by sequencing FAS in DNA from double-negative (DN) T cells, the pathognomonic T-cell subset in ALPS, in which the somatic events accumulated.
View Article and Find Full Text PDFTryptophan alleviates intestinal damage through regulating necroptosis and TLR4/NOD signaling pathways in pigs after lipopolysaccharide challenge.
Anim Biotechnol
December 2023
Maize Research Institute, Sichuan Agricultural University, Chengdu, Sichuan, China.
This study aimed to test the hypothesis that necroptosis, toll-like receptor 4 (TLR4)/nucleotide-binding oligomerization domain (NOD) signaling pathway in the jejunum of lipopolysaccharide (LPS)-challenged piglets are involved in the alleviation of intestinal injury and inflammation by tryptophan supplementation. Tryptophan supplementation has improved intestinal morphology. Also, tryptophan has been found to increase the mRNA and protein expression of tight junction proteins and decrease the expression of pro-inflammatory cytokines.
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