Volume 18 Issue 10, October 2017

Interferon-λ (IFN-λ) curbs neutrophil-mediated intestinal inflammation by diminishing the production of reactive oxygen species and subsequent oxidative stress. This regulatory process is unique to IFN-λ and is independent of interferon-induced transcription and translation programs.

T-bet⁺NKp46⁺ subsets of group 1 and group 3 innate lymphoid cells within the meninges initiate neuroinflammation in central nervous system (CNS)-demyelinating disease by regulating both the stability of pathogenic T-bet⁺ T cells and their access to the CNS.

Caveolin-1 has a critical role in orchestrating the membrane organization of B cells. In its absence, signaling via the B cell antigen receptor and B cell tolerance are impaired, which results in autoimmunity.

Kaplan reviews the development of skin-resident Langerhans cells and their unique functional roles that distinguish these cells from other skin antigen-presenting cells.

Lambrecht and Hammad discuss how microbial diversity or dysbiosis influences epithelial barrier tissues and the impact of such interactions on the development of allergic disease.

The effect of the cytokine IFN-λ in non-epithelial cells remains unclear. Zanoni and colleagues show that IFN-λ specifically activates a signaling pathway that diminishes the production of reactive oxygen species and degranulation in neutrophils.

Helicases are vital to the induction of antiviral responses. Cao and colleagues demonstrate that the helicase DDX46 is involved in the epigenetic regulation of select RNA species encoding antiviral molecules, which leads to the retention of the RNAs in the nucleus and thus blockade of their translation and the activity of the proteins encoded.

No response by an immune cell occurs in isolation but is instead the summation of multiple interacting signals. Ivashkiv and colleagues describe the epigenetic landscape that results from the integration of the inflammatory cytokines type I interferons and TNF.

Lazarevic and colleagues show that T-bet-dependent NKp46⁺ innate lymphoid cells reside within the meninges of the CNS and initiate meningeal inflammation, thereby facilitating T cell entry into parenchymal CNS tissues and contributing to neuroinflammation.

Targeting the transcription factor RORγt in autoimmunity could disrupt thymocyte development and lead to thymic lymphoma. Sun and colleagues identify a two-amino-acid substitution in RORγt that ‘preferentially’ disrupts T_H17 differentiation, not thymocyte development.

The molecular events that initiate lymphoid-lineage specification remain unidentified. Cumano and colleagues define the transcriptional signatures that characterize the loss of B cell or T cell potential.

Immature B cells are subject to tolerance mechanisms that prevent the expression of self-reactive BCRs. Minguet and colleagues identify the membrane protein caveolin-1 as a regulator of BCR spatial organization and signaling that enforces B cell tolerance.

Specialized populations of regulatory T cells inhabit tissues and maintain homeostasis, and assist with repair functions there. Feuerer and colleagues identify a genome-wide DNA-methylation landscape to define this specialized subset of cells.