Isaac J Jensen, Samantha N Jensen ... Vladimir P Badovinac
Sepsis-induced numerical loss of naive autoantigen-specific CD4 T cells reduces host capacity to develop autoimmune immune disease, thereby demonstrating an intriguing relationship between infection and autoimmune disease.
Damilola Pinheiro, Marie-Anne Mawhin ... Kevin J Woollard
In-silico modeling of gene and protein emergence reveals how colony-stimulating factors contributed to the evolution and functional adaptions observed in mammalian neutrophils.
Phosphorylation-mediated inactivation of pro-apoptotic BCL-2 family protein BAD confers the apoptosis resistance on synovial sublining macrophages, thereby contributing to the development of rheumatoid arthritis.
Kirsteen M Tullett, Peck Szee Tan ... Mireille H Lahoud
Dendritic cell recognition and processing of antigens from dead cells, utilising the Clec9A-damage recognition receptor, is controlled by a novel RNF41-ubiquitin-mediated regulatory pathway.
Sonya Kumar Bharathkar, Benjamin W Parker ... Beth M Stadtmueller
The structures of secretory and dimeric IgA reveal pseudosymmetric assemblies of two antibody monomers, in which possible positions of antigen-binding fragments and accessibility to receptor-binding sites are limited.
Cristina Alarcón-Vila, Alberto Baroja-Mazo ... Pablo Pelegrin
A murine model of sepsis shows that the purinergic P2X7 receptor controls the release of CD14 in extracellular vesicles playing a key role in cytokine production, bacterial clearance, and survival.
A new system to genetically label and manipulate plasma cells in vivo in their microenvironment resolves current technical limitations and reveals tissue-specific homeostatic population turnover.
Shubhanshi Trivedi, Daniel Labuz ... Daniel T Leung
Mucosal-associated invariant T (MAIT) cells, highly activated and dysfunctional in sepsis patients, contribute to tissue-specific cytokine responses that are protective against mortality during experimental sepsis.
