Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.

Background: Neutrophils are the most abundant leukocytes in human blood, and their recruitment is essential for innate immunity and inflammatory responses. The initial and critical step of neutrophil recruitment is their adhesion to vascular endothelium, which depends on G protein-coupled receptor (GPCR) triggered integrin inside-out signaling that induces β2 integrin activation and clustering on neutrophils. Kindlin-3 and talin-1 are essential regulators for the inside-out signaling induced β2 integrin activation.

Proinflammatory and cytotoxic CD38 HLA-DR effector memory CD8 T cells are peripherally expanded in human cardiac allograft vasculopathy.

Background: T cell mediated immunity is reported to play a pathogenic role in cardiac allograft vasculopathy (CAV) in heart transplant (HTx) patients. However, peripheral blood CD8 T cells have not been previously characterized in CAV. This study aimed to identify potentially pathogenic circulating CD8 T cell populations in high grade CAV patients using cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq).

PD-1 and CD73 on naive CD4 T cells synergistically limit responses to self.

Vaccination with self- and foreign peptides induces weak and strong expansion of antigen-specific CD4 T cells, respectively, but the mechanism is not known. In the present study, we used computational analysis of the entire mouse major histocompatibility complex class II peptidome to test how much of the naive CD4 T cell repertoire specific for self-antigens was shaped by negative selection in the thymus and found that negative selection only partially explained the difference between responses to self and foreign. In naive uninfected and unimmunized mice, we identified higher expression of programmed cell death protein 1 (PD-1) and CD73 mRNA and protein on self-specific CD4 T cells compared with foreign-specific CD4 T cells.

Olfr2-positive macrophages originate from monocytes proliferate in situ and present a pro-inflammatory foamy-like phenotype.

Aims: Olfactory receptor 2 (Olfr2) has been identified in a minimum of 30% of vascular macrophages, and its depletion was shown to reduce atherosclerosis progression. Mononuclear phagocytes, including monocytes and macrophages within the vessel wall, are major players in atherosclerosis. Single-cell RNA sequencing studies revealed that atherosclerotic artery walls encompass several monocytes and vascular macrophages, defining at least nine distinct subsets potentially serving diverse functions in disease progression.