The network structural entropy for single-cell RNA sequencing data during skin aging DOI Creative Commons
Zhilong Liu, Hai Lin, Xiang Li

и другие.

Briefings in Bioinformatics, Год журнала: 2024, Номер 26(1)

Опубликована: Ноя. 22, 2024

Abstract Aging is a complex and heterogeneous biological process at cellular, tissue, individual levels. Despite extensive effort in scientific research, comprehensive understanding of aging mechanisms remains lacking. This study analyzed aging-related gene networks, using single-cell RNA sequencing data from >15 000 cells. We constructed correlation network, integrating expressions into the weights network edges, ranked importance random walk model to generate matrix. unsupervised method improved clustering performance cell types. To further quantify complexity networks during aging, we introduced structural entropy. The findings our reveal that overall entropy increases aged cells compared young However, changes varied greatly within different subtypes. Specifically, among various types may increase, remain unchanged, or decrease. wide range be closely related their functions, highlighting cellular heterogeneity potential key reconfigurations. Analyzing provides insights molecular behind aging. offers new evidence theoretical support for functions

Язык: Английский

RIPK1 protects naive and regulatory T cells from TNFR1-induced apoptosis DOI Creative Commons
Jelle Huysentruyt, Wolf Steels, Mario Pérez

и другие.

Cell Death and Differentiation, Год журнала: 2024, Номер 31(6), С. 820 - 832

Опубликована: Май 11, 2024

Abstract The T cell population size is stringently controlled before, during, and after immune responses, as improper death regulation can result in autoimmunity immunodeficiency. RIPK1 an important regulator of peripheral survival homeostasis. However, whether different subsets show a differential requirement for which programmed pathway they engage vivo remains unclear. In this study, we demonstrate that conditional ablation Ripk1 conventional cells ( ΔCD4 ) causes lymphopenia, witnessed by profound loss naive CD4 + , CD8 FoxP3 regulatory cells. Interestingly, mice appear to undergo selective pressure retain expression following activation. Mixed bone marrow chimeras revealed competitive disadvantage naive, effector, memory lacking RIPK1. Additionally, tamoxifen-induced deletion CD4-expressing adult life confirmed the importance post-thymic K45A showed no change subsets, demonstrating lymphopenia was due scaffold function rather than its kinase activity. Enhanced numbers expressed proliferation marker Ki-67 despite single-cell RNA sequencing cell-specific transcriptomic alterations were reverted additional caspase-8 deficiency. Furthermore, Casp8 Tnfr1 −/− double-knockout rescued revealing RIPK1-deficient specifically die from TNF- caspase-8-mediated apoptosis vivo. Altogether, our findings emphasize essential role maintaining compartment preventing TNFR1-induced apoptosis.

Язык: Английский

Процитировано

4

Everything everywhere all at once: Unraveling the waves of aging DOI
Jose Ignacio Escrig, Marı́a Mittelbrunn

Immunity, Год журнала: 2025, Номер 58(2), С. 276 - 278

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

0

Targeting T-cell Aging to Remodel the Aging Immune System and Revitalize Geriatric Immunotherapy DOI Creative Commons
Chen Mi, Su Zhou, Jianxin Xue

и другие.

Aging and Disease, Год журнала: 2025, Номер unknown, С. 0 - 0

Опубликована: Янв. 1, 2025

The aging immune system presents profound challenges, notably through the decline of T cell function, which is critical for effective responses. As age-related changes lead to diminished diversity and heighten immunosuppressive environments, older individuals face increased susceptibility infections, autoimmune diseases, reduced efficacy immunotherapies. This review investigates intricate mechanisms by drives immunosenescence, including suppression, evasion, antigen reactivity, overexpression checkpoint molecules. By delving into innovative therapeutic strategies aimed at rejuvenating populations modifying immunological landscape, we highlight potential enhancing resilience in elderly. Ultimately, our goal outline actionable pathways restoring thereby improving health outcomes facing decline.

Язык: Английский

Процитировано

0

RIPK1 ablation in T cells results in spontaneous enteropathy and TNF-driven villus atrophy DOI Creative Commons
Jelle Huysentruyt, Wolf Steels, Mario Pérez

и другие.

EMBO Reports, Год журнала: 2025, Номер unknown

Опубликована: Апрель 30, 2025

RIPK1 is a crucial regulator of cell survival, inflammation and death. Human deficiency leads to early-onset intestinal peripheral T imbalance, though its role in αβT cell-mediated homeostasis remains unclear. In this study, we demonstrate that mice with ablation conventional cells (Ripk1ΔCD4) developed severe small pathology characterized by elongation, crypt hyperplasia, duodenum-specific villus atrophy. Using mixed bone marrow chimeras reveals survival disadvantage compared γδT the intestine. Broad-spectrum antibiotic treatment ameliorates hyperplasia prevents atrophy persists. Conversely, crossing Ripk1ΔCD4 TNF receptor 1 Tnfr1-/- knockout rescues but not elongation. Finally, combined Ripk1∆CD4 Casp8∆CD4 fully pathology, revealing apoptosis drives enteropathy. These findings RIPK1-mediated essential for proximal homeostasis. mice, imbalanced compartment microbiome-mediated elongation TNF-driven

Язык: Английский

Процитировано

0

Excessive apoptosis of Rip1‐deficient T cells leads to premature aging DOI Open Access
Lingxia Wang, Xixi Zhang,

Haiwei Zhang

и другие.

EMBO Reports, Год журнала: 2023, Номер 24(12)

Опубликована: Ноя. 15, 2023

Язык: Английский

Процитировано

7

Not to be and how not to be: the questions of Tregs controlled by RIPK1 DOI

Zhengcai Peng,

Huiyuan Zhang, Hongbo Hu

и другие.

Cellular and Molecular Immunology, Год журнала: 2024, Номер 21(2), С. 205 - 206

Опубликована: Янв. 15, 2024

Язык: Английский

Процитировано

0

The network structural entropy for single-cell RNA sequencing data during skin aging DOI Creative Commons
Zhilong Liu, Hai Lin, Xiang Li

и другие.

Briefings in Bioinformatics, Год журнала: 2024, Номер 26(1)

Опубликована: Ноя. 22, 2024

Abstract Aging is a complex and heterogeneous biological process at cellular, tissue, individual levels. Despite extensive effort in scientific research, comprehensive understanding of aging mechanisms remains lacking. This study analyzed aging-related gene networks, using single-cell RNA sequencing data from >15 000 cells. We constructed correlation network, integrating expressions into the weights network edges, ranked importance random walk model to generate matrix. unsupervised method improved clustering performance cell types. To further quantify complexity networks during aging, we introduced structural entropy. The findings our reveal that overall entropy increases aged cells compared young However, changes varied greatly within different subtypes. Specifically, among various types may increase, remain unchanged, or decrease. wide range be closely related their functions, highlighting cellular heterogeneity potential key reconfigurations. Analyzing provides insights molecular behind aging. offers new evidence theoretical support for functions

Язык: Английский

Процитировано

0