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Brief Definitive Report

Neuronal activity promotes the release of extracellular tau in vivo.

Rapamycin modulates the ability of the vascular endothelium to mediate inflammation by inhibiting mTORC2 and reducing TNF-induced VCAM-1 expression.

Epitope-specific antibody responses recognized by germline-encoded structures are of significant relevance for the development of autoantibody-mediated autoimmune diseases.


B cells expressing the MYD88 L265P mutation undergo rapid TLR ligand-independent proliferation that is self-limiting unless apoptosis is opposed.

The protein tyrosine phosphatase PTP1B regulates co-receptor signaling on B cells and thus controls B cell autoimmunity.

Intravital visualization of autoimmune-induced tissue damage and Treg cell protection shows contact-based immune cell interactions and growth of bystander tissue cells in pancreatic islet grafts.

The development of serrated polyps in the cecum is driven by the interplay among genetic changes in the host, an inflammatory response, and a host-specific microbiota.

Co-targeting of both de novo and salvage pathways for dCTP biosynthesis shows efficacy in T-ALL and B-ALL.

Upon transplant, functional HSC clones preferentially expand in certain skeletal locations, exhibiting only limited migration toward other niches.

Elevated kallikrein 5 expression is sufficient to trigger the majority of the clinical hallmarks of Netherton syndrome.

The transcription factor Blimp-1 represses PD-1 expression in effector CD8+ T cells during acute LCMV infection.

Loss of the Tec family kinase Itk results in a bias to FoxP3+ Treg cell differentiation and reduced TCR-induced phosphorylation of mTOR targets.

T cell–specific NFAT2 deletion results in reduced CXCR5+ follicular regulatory T cells, leading to uncontrolled germinal center responses and humoral autoimmunity.

Mutually exclusive expression of T-bet and Eomes drives the development of distinct NK cell lineages with complementary functions.

Disruption of endothelial adherens junctions in response to inflammatory signals is mediated by the heterotrimeric G protein Gα13, which binds to VE-cadherin and induces VE-cadherin internalization through Src-dependent signaling pathway.

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