Controlled neo-glycosylation of antigens can influence intracellular routing of antigens and the nature and strength of immune response, and should therefore be considered as a major determinant in the design of vaccines against cancer and infectious diseases.

TET methylcytosine oxidases cooperate with B lineage-specific transcription factors to promote immunoglobulin gene rearrangement by depositing 5hmC, facilitating DNA demethylation and increasing chromatin accessibility at enhancers.

HMGB1 drives the development of paucigranulocytic asthma in RAGE deficient mice.

Tumor immunogenicity is quantified with a novel method, and the resulting tumor immunogenicity score is an effective tumor-inherent biomarker for prediction of response to immune checkpoint inhibitors.

Reprogramming of transcription factors by PRR-independent (cAMP) and PRR-dependent (curdlan) signaling induces new dendritic cell subset.

The heterogeneity of immune cell types in glioblastoma tumors depends on the tumor's genetic make-up and treatment status and is an incompletely mined source of novel therapeutic targets.

Multiplexing and digital analysis of melanoma tissue describe functionally the microenvironment associated with brisk/non-brisk infiltrates and expose the functional incongruences of this morphological classification currently in use for tumor-infiltrating lymphocytes.

Older individuals have impaired conventional dendritic cell and T follicular helper cell formation upon vaccination, which can be rescued by treatment with a TLR7 agonist.

Cancer systems immunology is a highly interdisciplinary field that is advancing our ability to understand and predict the complex behavior that orchestrates the interplay between tumors and the immune system.

Notch signaling alters TLR-induced inflammation by skewing monocyte cell fate toward patrolling monocyte differentiation at the expense of macrophage cell fate.