By comparing different subsets in mouse inducible Tfh (iTfh) cells and human circulating Tfh (cTfh) cells after vaccination, Tfh17 cells were found to be better than Tfh1 or Tfh2 cells in maintenance and support immunological memory of humoral immunity.

A chemical biology approach has identified the kinase DYRK1A as a new regulator of the inflammatory response.

Cellular immunological and biochemical analyses reveal how decoy IL-1RII is induced by human CD4⁺ T cells upon TCR-stimulation and regulates the Th17-Treg balance by modulating IL-1β responsiveness in IL-1RI⁺ cells.

The expression of DECTIN-2 family C-type lectin receptors on macrophages and monocytes is inhibited by the Th2 cytokine IL-4, which suggests a mechanism for inhibition of Th17 responses to MINCLE-dependent vaccination responses by underlying helminth infection.

The acquisition of cytotoxic function by human CD4 T cells is an integral part of the T helper 1 differentiation pathway and is limited by the transcription factor ThPOK.

Gnotobiotic and conventional mouse models of the IBD ATG16L1T300A SNP reveal gene-microbiota-immune interactions.

The accumulation of carbon black nanoparticles in smokers' lungs causes sterile inflammation, double-strand DNA breaks and emphysema.

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

Development of a robust Th1 response to infection against an intracellular parasite requires T-cell intrinsic MyD88 signaling, mostly through the upstream IL-18 receptor, for the induction of genes involved in proliferation, cytokine production and migration.