Contents
June 2017
Vol 2, Issue 12
Vol 2, Issue 12
Research Articles
- Donor SIRPα polymorphism modulates the innate immune response to allogeneic grafts
Detection of nonself SIRPα by CD47 triggers an innate immune response to allografts in mice that lack T, B, and NK cells.
- Suppression by human FOXP3+ regulatory T cells requires FOXP3-TIP60 interactions
Targeting the FOXP3-TIP60 interaction may modulate Treg activity in IPEX and other autoimmune and inflammatory diseases.
- Memory-phenotype CD4+ T cells spontaneously generated under steady-state conditions exert innate TH1-like effector function
Memory-phenotype CD4+ T cells provide early, foreign antigen–independent innate resistance to TH1-inducing pathogens.
- Citrullination of NF-κB p65 promotes its nuclear localization and TLR-induced expression of IL-1β and TNFα
Heightened citrullination promotes the expression of inflammatory cytokines in rheumatoid arthritis.
- Plasmodium products persist in the bone marrow and promote chronic bone loss
Plasmodium infection causes chronic inflammation and bone loss through Plasmodium product accumulation in the bone marrow.
- Resident memory CD8+ T cells in the upper respiratory tract prevent pulmonary influenza virus infection
Nasal tissue–resident memory T cells block influenza virus transmission to the lung, preventing severe pulmonary disease.
- Human thymoproteasome variations influence CD8 T cell selection
Genetic variations in antigen-peptide processing machinery influence T cell repertoire selection and susceptibility to autoimmune disease.
Editors' Choice
- PD-1 blockade: It’s what’s for dinner
Tumor-associated macrophages limit the efficacy of programmed cell death 1 (PD-1) blockade through an FcγR-dependent clearance mechanism.
- Tumor immune landscape paintings from the CyTOF period
Early lung cancer patients harbor cancer-permissive innate immunity in the tumor microenvironment.
About The Cover
ONLINE COVER Plasmodium Infection Cuts to the Bone. Shown are femurs from naïve (left) and Plasmodium yoelii–infected (right) mice. Lee et al. report that Plasmodium infection causes chronic inflammation and bone loss through Plasmodium product accumulation in the bone marrow. [CREDIT: LEE ET AL./SCIENCE IMMUNOLOGY]