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Dr. Tuveson and colleagues provide a comprehensive review on the fundamental role of cancer-associated fibroblasts in shaping the tumor microenvironment and promoting tumor initiation and progression.

Brief Definitive Report

Gata6 regulates differentiation, metabolism and survival of peritoneal macrophages.


Phagocytic monocyte-derived macrophages associate with the nodes of Ranvier and initiate demyelination while microglia clear debris and display a suppressed metabolic gene signature in EAE.

Acid sphingomyelinase activity is increased in brain and plasma of mice and patients with Alzheimer’s disease and its inhibition represents a potential new therapeutic intervention for this disease.

Intestinal CX3CR1+ mononuclear phagocytes regulate ILC3 in vivo in response to colitis associated microbial signals.

A novel MAIT cell antagonist, Ac-6-FP, stabilizes MR1 and can inhibit MAIT cell activation with the flexible TCR β-chain serving to fine-tune the affinity of the TCR for antigen-MR1 complexes.

MAIT cells can discriminate between pathogen-derived ligands in a clonotype-dependent manner, and the TCR repertoire is distinct within individuals, indicating that the MAIT cell repertoire is shaped by prior microbial exposure.

Resident lymph node DCs rapidly locate viral influenza antigen to drive early activation of T cells, resulting in germinal center formation and B cell memory.

Transcriptional cofactor of the ETO family Mtg16 promotes pDCs and restricts cDC differentiation in part by repressing Id2.

Antibodies can regulate the quality and functionality of a subset of antiviral CD8+ T cell memory responses to influenza by promoting sustained DC antigen presentation during the contraction phase of primary responses.

Eosinophil degranulation of peroxidase promotes DC activation and mobilization from the intestine to LNs to induce Th2 immunity and food allergy.

Macrophage-derived 18-HEPE protects mice from cardiac remodeling by preventing proinflammatory activation of cardiac fibroblasts and subsequent fibrosis.

TPL2 is required for Th17-mediated neuroinflammation during EAE by regulating the TAK1 signaling axis downstream of the IL-17R in astrocytes.

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