March 2014 | Volume 211, No. 3
Brief Definitive Reports
- Rapamycin antagonizes TNF induction of VCAM-1 on endothelial cells by inhibiting mTORC2
Rapamycin modulates the ability of the vascular endothelium to mediate inflammation by inhibiting mTORC2 and reducing TNF-induced VCAM-1 expression.
- Epitope-specific antibody response is controlled by immunoglobulin VH polymorphisms
Epitope-specific antibody responses recognized by germline-encoded structures are of significant relevance for the development of autoantibody-mediated autoimmune diseases.
- Consequences of the recurrent MYD88L265P somatic mutation for B cell tolerance
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 is a negative regulator of CD40 and BAFF-R signaling and controls B cell autoimmunity
The protein tyrosine phosphatase PTP1B regulates co-receptor signaling on B cells and thus controls B cell autoimmunity.
- Real-time immune cell interactions in target tissue during autoimmune-induced damage and graft tolerance
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.
- Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice
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.
- Asymmetry in skeletal distribution of mouse hematopoietic stem cell clones and their equilibration by mobilizing cytokines
Upon transplant, functional HSC clones preferentially expand in certain skeletal locations, exhibiting only limited migration toward other niches.
- Transgenic kallikrein 5 mice reproduce major cutaneous and systemic hallmarks of Netherton syndrome
Elevated kallikrein 5 expression is sufficient to trigger the majority of the clinical hallmarks of Netherton syndrome.
- Blimp-1 represses CD8 T cell expression of PD-1 using a feed-forward transcriptional circuit during acute viral infection
The transcription factor Blimp-1 represses PD-1 expression in effector CD8+ T cells during acute LCMV infection.
- Itk-mediated integration of T cell receptor and cytokine signaling regulates the balance between Th17 and regulatory T cells
Loss of the Tec family kinase Itk results in a bias to FoxP3+ Treg cell differentiation and reduced TCR-induced phosphorylation of mTOR targets.
- Follicular regulatory T cells control humoral autoimmunity via NFAT2-regulated CXCR5 expression
T cell–specific NFAT2 deletion results in reduced CXCR5+ follicular regulatory T cells, leading to uncontrolled germinal center responses and humoral autoimmunity.
- T-bet and Eomes instruct the development of two distinct natural killer cell lineages in the liver and in the bone marrow
Mutually exclusive expression of T-bet and Eomes drives the development of distinct NK cell lineages with complementary functions.
- Evidence of a common mechanism of disassembly of adherens junctions through Gα13 targeting of VE-cadherin
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.