Results 51 to 60 of about 121,779 (302)

Innate immune evasion by filoviruses

Virology, 2015
Ebola viruses and Marburg viruses, members of the filovirus family, cause severe hemorrhagic fever. The ability of these viruses to potently counteract host innate immune responses is thought to be an important component of viral pathogenesis. Several mechanisms of filoviral innate immune evasion have been defined and are reviewed here.
openaire   +3 more sources

The pan-cancer landscape of crosstalk between epithelial-mesenchymal transition and immune evasion relevant to prognosis and immunotherapy response

npj Precision Oncology, 2021
An emerging body of evidence has recently recognized the coexistence of epithelial-mesenchymal transition (EMT) and immune response. However, a systems-level view and survey of the interplay between EMT and immune escape program, and their impact on ...
Guangyu Wang, Dandan Xu, Zicheng Zhang, Xinhui Li, Jiaqi Shi, Jie Sun, Huan-Zhong Liu, Xiaobo Li, Meng Zhou, Tongsen Zheng   +9 more
doaj   +1 more source

From omics to AI—mapping the pathogenic pathways in type 2 diabetes

FEBS Letters, EarlyView.
Integrating multi‐omics data with AI‐based modelling (unsupervised and supervised machine learning) identify optimal patient clusters, informing AI‐driven accurate risk stratification. Digital twins simulate individual trajectories in real time, guiding precision medicine by matching patients to targeted therapies.
Siobhán O'Sullivan, Lu Qi, Pierre Zalloua   +2 more
wiley   +1 more source

Response to neoadjuvant chemotherapy in early breast cancers is associated with epithelial–mesenchymal transition and tumor‐infiltrating lymphocytes

Molecular Oncology, EarlyView.
Epithelial–mesenchymal transition (EMT) and tumor‐infiltrating lymphocytes (TILs) are associated with early breast cancer response to neoadjuvant chemotherapy (NAC). This study evaluated EMT and TIL shifts, with immunofluorescence and RNA sequencing, at diagnosis and in residual tumors as potential biomarkers associated with treatment response.
Françoise Derouane, Jérôme Ambroise, Cédric van Marcke, Mieke Van Bockstal, Martine Berlière, Christine Galant, Hélène Dano, Médina Lougué, Elena Benidovskaya, Guy Jerusalem, Vincent Bours, Claire Josse, Jérôme Thiry, Aurélie Daumerie, Caroline Bouzin, Cyril Corbet, François P. Duhoux   +16 more
wiley   +1 more source

TOMM20 as a driver of cancer aggressiveness via oxidative phosphorylation, maintenance of a reduced state, and resistance to apoptosis

Molecular Oncology, EarlyView.
TOMM20 increases cancer aggressiveness by maintaining a reduced state with increased NADH and NADPH levels, oxidative phosphorylation (OXPHOS), and apoptosis resistance while reducing reactive oxygen species (ROS) levels. Conversely, CRISPR‐Cas9 knockdown of TOMM20 alters these cancer‐aggressive traits.
Ranakul Islam, Megan E. Roche, Zhao Lin, Diana Whitaker‐Menezes, Victor Diaz‐Barros, Eurico Serrano, Maria Paula Martinez Cantarin, Nancy J. Philp, Atrayee Basu Mallick, Ubaldo Martinez‐Outschoorn   +9 more
wiley   +1 more source

Vaccination and the dynamics of immune evasion [PDF]

Journal of The Royal Society Interface, 2006
Vaccines exert strong selective pressures on pathogens, favouring the spread of antigenic variants. We propose a simple mathematical model to investigate the dynamics of a novel pathogenic strain that emerges in a population where a previous strain is maintained at low endemic level by a vaccine.
Bryan T. Grenfell, Olivier Restif
openaire   +3 more sources

Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal‐like and malignant urothelial cells

Molecular Oncology, EarlyView.
Loss of the frequently mutated chromatin remodeler ARID1A, a subunit of the SWI/SNF cBAF complex, results in less open chromatin, alternative splicing, and the failure to stop cells from progressing through the cell cycle after DNA damage in bladder (cancer) cells. Created in BioRender. Epigenetic regulators, such as the SWI/SNF complex, with important
Rebecca M. Schlösser, Florian Krumbach, Eyleen Corrales, Geoffroy Andrieux, Christian Preisinger, Franziska Liss, Alexandra Golzmann, Melanie Boerries, Kerstin Becker, Ruth Knüchel, Stefan Garczyk, Bernhard Lüscher   +11 more
wiley   +1 more source

CoCl2‐induced glioma hypoxia environment enhances CD47‐SIRPα to promote tumor immune evasion

MedComm – Oncology
Elevated levels of tumor‐associated macrophages and microglia in the immune microenvironment of malignant gliomas promote tumor growth and progression.
Xiangfei Ding, Jianbing Hou, Xiaosong Hu, Wen Peng, Yongsen Li, Gaichao Zhao, Hongjuan Cui, Zonghui Wu, Ping Liang   +8 more
doaj   +1 more source

Innate Immune Evasion of Alphaherpesvirus Tegument Proteins

Frontiers in Immunology, 2019
Alphaherpesviruses are a large family of highly successful human and animal DNA viruses that can establish lifelong latent infection in neurons. All alphaherpesviruses have a protein-rich layer called the tegument that, connects the DNA-containing capsid
Linjiang Yang, Linjiang Yang, Linjiang Yang, Mingshu Wang, Mingshu Wang, Mingshu Wang, Anchun Cheng, Anchun Cheng, Anchun Cheng, Qiao Yang, Qiao Yang, Qiao Yang, Ying Wu, Ying Wu, Ying Wu, Renyong Jia, Renyong Jia, Renyong Jia, Mafeng Liu, Mafeng Liu, Mafeng Liu, Dekang Zhu, Dekang Zhu, Dekang Zhu, Shun Chen, Shun Chen, Shun Chen, Shaqiu Zhang, Shaqiu Zhang, Shaqiu Zhang, Xinxin Zhao, Xinxin Zhao, Xinxin Zhao, Juan Huang, Juan Huang, Juan Huang, Yin Wang, Yin Wang, Yin Wang, Zhiwen Xu, Zhiwen Xu, Zhiwen Xu, Zhengli Chen, Zhengli Chen, Zhengli Chen, Ling Zhu, Ling Zhu, Ling Zhu, Qihui Luo, Qihui Luo, Qihui Luo, Yunya Liu, Yunya Liu, Yunya Liu, Yanling Yu, Yanling Yu, Yanling Yu, Ling Zhang, Ling Zhang, Ling Zhang, Bin Tian, Bin Tian, Leichang Pan, Leichang Pan, Mujeeb Ur Rehman, Mujeeb Ur Rehman, Xiaoyue Chen, Xiaoyue Chen, Xiaoyue Chen   +68 more
doaj   +1 more source

Mechanism of Borrelia immune evasion by FhbA-related proteins.

PLoS Pathogens, 2022
Immune evasion facilitates survival of Borrelia, leading to infections like relapsing fever and Lyme disease. Important mechanism for complement evasion is acquisition of the main host complement inhibitor, factor H (FH). By determining the 2.2 Å crystal
Konstantin Kogan, Karita Haapasalo, Tommi Kotila, Robin Moore, Pekka Lappalainen, Adrian Goldman, Taru Meri   +6 more
doaj   +1 more source