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Pulmonary fibrosis is a complex and heterogeneous disease; a more detailed and integrated understanding of the cellular and molecular mechanisms influencing its pathogenesis will aid the design of new therapies.

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VEGF deprivation induces Bim expression in tumor endothelial cells, and Bim is needed for anti-VEGF–driven endothelial cell death and tumor shrinkage.

Somatic STAT3 mutations present in a subset of inflammatory hepatocellular adenomas result in the generation of constitutively active STAT3 proteins that homodimerize independently of IL-6 stimulation.

HIF1α induction by mTOR represents a metabolic checkpoint for the differentiation of TH17 and Treg cells.

Bcl-6 expression in CD4+ T cells is required to generate extrafollicular antibody responses.


Next generation sequencing and copy number analysis provide insights into the complexity of the CLL coding genome, and reveal an association between NOTCH1 mutational activation and poor prognosis.

Deletion of E4F1 inflicts mitochondrial damage and oxidative stress on murine and human myeloid leukemia cells but not healthy macrophages.

Structure–function analysis and mathematical modeling reveal insight into the mechanisms through which conserved HIV-1 gp120 epitopes are masked in the HIV-1 envelope trimer.

CD28 signaling is essential for maintenance of long-term antigen-specific antibody production and for persistence of plasma cells in the bone marrow of mice.

CIN85 transduces B cell receptor signals to IKK-β, and its expression in B cells is essential for T cell–independent type II antibody responses in mice.

Hyaluronan synthase 2 and CD44 are required for severe lung fibrosis in response to bleomycin.

Mice lacking FoxM1 specifically in progenitor-like type II alveolar epithelial cells exhibit defective alveolar barrier repair after microbe-induced lung injury.

Identification of a population of Foxp3-expressing suppressive macrophages.

Subimmunogenic vaccination with an agonist mimetope of insulin converts naive T cells into regulatory T cells and prevents type 1 diabetes in NOD mice.

As shown in humanized mice, a population of Vγ9Vδ2 T cells can reduce the severity and mortality of disease caused by infection with human and avian influenza viruses.

SOCS2-deficient T cells more readily produce Th2 cytokines, and SOCS2-deficient mice exhibit exacerbated atopic dermatitis and allergic airway inflammation.

Toxoplasma virulence factor ROP18 targets endoplasmic reticulum–bound transcription factor ATF6β in the host cell, leading to the detrimental loss of ATF6β through proteasome-dependent degradation.

Expression of a bacterial transporter protein in Toxoplasma gondii results in parasite susceptibility to Formidomycin, a drug targeting isoprenoid precursor synthesis.

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