Skip to Main Content

Advertisement

Issues

  • Cover Image

    Cover Image

    issue cover

    ON THE COVER
    Heaton et al. find that a population of lung cells, known as club cells, become infected with influenza A virus but ultimately survive the infection. The club cells continue to have an inflammatory signature after viral clearance that prolongs lung pathology. The bottom portion of the cover image depicts healthy uninfected lung tissue, the middle shows damage inflicted by flu infection, and the top section shows reduced pathology after depletion of previously infected club cells. Artwork by Emilie Clark (emilie@emilieclark.com).
    See page 1707

  • PDF Icon PDF LinkTable of Contents
  • PDF Icon PDF LinkEditorial Board
ISSN 0022-1007
EISSN 1540-9538
In this Issue

Insights

Brief Definitive Report

Club cells are infected by influenza virus, survive acute infection, and establish a proinflammatory environment that contributes to lung pathology. Depletion of club cells reduces lung tissue damage associated with flu infection.

RHEX is a novel target of the human erythropoietin receptor, and modulator of EPO-dependent red cell production.

Nfil3 is critical for normal development of innate lymphoid cell (ILC) progenitors. Nfil3-deficient mice have severely reduced lung and visceral adipose tissue ILC2s and gut-associated ILC3s, and compromised innate immunity to acute bacterial infection.

Loss of Nfil3 selectively reduces Peyer’s patch formation, impairing recruitment and distribution of lymphocytes and compromising immune responses to inflammatory and infectious agents.

Article

Mice lacking the small GTPase Rap1b exhibit enhanced neutrophil recruitment to inflamed lungs and susceptibility to endotoxin shock via enhance PI3K-Akt activation.

In vivo deletion of USP3, a deubiquitinating enzyme involved in DNA damage repair, increases the incidence of spontaneous cancer and impairs the proliferation and repopulation ability of HSCs.

PI3Kγ plays a major role in the initiation and progression of intimal hyperplasia by specifically modulating Th1 cytokines leading to CXCL10 and RANTES production by smooth muscle cells.

A novel site-targeted murine complement inhibitor, CR2-CD59, specifically inhibits the terminal membrane attack complex. This inhibitor dissects the complement pathway to protect against liver injury while promoting regeneration in mouse models of liver resection and acute liver failure.

The transcriptional regulator Blimp-1 is absolutely required for IL-10 production in Th1 cells and limits inflammatory effector T cell responses downstream of IL-12 and IL-27.

Within the human TCR-α/δ locus, ordered rearrangements requires RUNX1, which binds to the Dδ2-23RSS and interacts with RAG1 to enhance RAG1 deposition at this site. Absence of this RUNX1 binding site in the homologous murine Dδ1-23RSS offers an explanation for the lack of ordered TCR-δ gene assembly in mice.

Schneider-Hohendorf describe expression of adhesion molecules MCAM and PSGL-1 on human CD4+ T cells and Th17 T cells in multiple sclerosis patients under long-term natalizumab treatment. The authors identify that despite blockade of VLA-4, MCAM+ T cells can migrate through the blood–brain barrier to access the CNS through PSGL-1 and MCAM.

Immunosuppression from amyloidogenic peptides arises from two pathways, expression of type 1 IFN by pDCs and reduced expression of IFN-γ, TNF, and IL-6, which together modulate the signs of both Th1- and Th17-induced EAE.

A novel isoform of Sox5, Sox5t, and c-Maf activate RORγt to induce Th17 cells. Sox5−/− mice exhibit impaired Th17 differentiation and are thus resistant to EAE and delayed-type hypersensitivity.

Protective immunity to protein vaccines is controlled by Flt3L-dependent classical LN-resident dendritic cells, and dampened by migratory dendritic cells.

An antibody directed against the O-antigen of Pseudomonas aeruginosa LPS can block complement-mediated bacterial killing and contributes to the severity of respiratory infection.

T reg cells effectively maintain CD8 T cell exhaustion during chronic LCMV infection, but blockade of PD-1 is critical for elimination of infected cells.

Retraction

Close Modal
This Feature Is Available To Subscribers Only

Sign In or Create an Account

Close Modal
Close Modal