Dean Sheppard

The paper shows that blocking integrin αvβ8 suppresses TGFβ in tumor-draining lymph nodes and enhances DC-T cell activation, offering a new immunotherapy strategy distinct from TGFβ ligand blockade.

The paper identifies IAV-driven fibroblast states and shows that loss of TGFβ signaling enhances immuno-modulatory fibroblasts, supporting T2-Tregs to improve lung outcomes.

This study identifies EBF1 and ITGB8 as key regulators of BM fibrosis in myelofibrosis and shows their inhibition reduces disease features in mouse models.

The paper identifies MMP1high basal cells derived from alveolar type II cells that contribute to microcyst formation in IPF, suggesting a therapeutic target through MMP inhibition or WNT modulation.

This study identifies dynamic fibroblast-immune interactions that regulate CNS wound healing and neuroinflammation after brain injury.

This paper engineers T cells with synthetic receptors that activate only in the lung, demonstrating RAGE as a lung-specific target for targeted therapies.

This study shows that fibroblast proliferation drives pulmonary fibrosis and that targeting this process could be a new therapeutic strategy.

This study identifies β-III tubulin as a marker for anti-fibrotic pericytes in pulmonary fibrosis and shows that Tuj1-expressing pericytes release CXCL10 to inhibit pro-fibrotic macrophage differentiation.

This study identifies impaired myofibroblast proliferation as a central feature of alveolar simplification in BPD using single-cell RNA sequencing and pharmacologic approaches.

This paper shows IL-13 and IL-17A activate β1 integrins through an NF-κB/Rho kinase/PIP5K1γ pathway, enhancing force transmission in airway smooth muscle and linking this to asthma pathology.

This study uses longitudinal meta-regression to examine how DNA methylation effects on child health outcomes vary by timing, finding larger effects in childhood but noisier associations and time-specific signals.

This study shows that inhibiting IRE1α kinase/RNase reduces lung fibrosis in mice by blocking the terminal UPR, with two compounds demonstrating efficacy in preventing and reversing fibrosis.