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Brief Definitive Report

IL-21 is a key CD4+ T cell–derived inflammatory factor that contributes to increased early ischemic tissue injury.

Targeting Csnk1a1 provides a potential therapeutic approach for AML associated with nonmutated Tp53.

Novel A-to-I RNA editing in the coding sequence of RHOQ leads to an amino acid substitution that promotes invasion in colorectal cancer.

Interactions between cell adhesion molecules CRTAM and Cadm1 regulate the residency and maintenance of CD4+CD8+ and CD4+ T cells in the gut that can influence the immune response to infection.

E4bp4 is required for commitment to the NK lineage and promotes NK development by directly regulating the expression of Eomes and Id2.

The requirements for BALT formation are pathogen-dependent and, in the absence of FDC maturation, IL-17 can drive BALT formation via CXCL12 B cell recruitment.


Salmonella lacking the TCA enzyme aconitase trigger NLRP3 inflammasome activation in infected macrophages, leading to elevated inflammatory responses and reduced virulence.

BRAF-V600E expression is identified in hematopoietic progenitor and precursor myeloid dendritic cells in patients with high-risk LCH, and enforced expression of BRAF-V600E in CD11c+ cells recapitulates a high-risk LCH-like phenotype in mice.

The endocytosis regulator dynamin 2 is required for the regulation of S1PR1 internalization and continued S1PR1 signaling in low S1P environments.

Two interleukin-7 receptor mutants identified in human early T cell precursor leukemia are sufficient to induce disease in mice when expressed in primitive, Arf-null thymocytes.

In Special Collection:
2018 Nobel Prize Collection

CTLA-4 blockade leads to enhanced activation of tumor-reactive T cells with concomitant up-regulation of ICOS, thus enabling their responses to be enhanced by ICOS engagement.

EAT-2 promotes NK cell activation by linking SLAM family receptors to PLCγ, Ca++, and Erk signals to promote polarization and exocytosis of cytolytic granules towards target cells.

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