Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Clostridium difficileinfection induces the expression of interleukin-22, which regulates the complement system to eliminate systemically translocated pathobionts.
Respiratory infection with influenza virus causes intestinal symptoms through the specific recruitment of lung-induced CD4+T cells to the intestinal mucosa.
This Review describes the biology of the interleukin-20 (IL-20) subfamily of cytokines. The authors detail the cellular sources and targets of these cytokines, and explain their key roles in promoting immunity to infections and driving tissue repair. They also discuss the emerging roles for IL-20 subfamily cytokines in metabolism and tumour immunology.
Being able to useDrosophila melanogaster to study immunity on a whole-organism level is proving to be highly valuable in deciphering the links between systemic metabolic and hormonal changes and the immune response. Here, the authors describe the insights gained so far into organism-wide immune regulation and the future directions for research in D. melanogaster.
Recent studies have shown that complement activation is not confined to the serum but also occurs within cellular compartments. This has led to an emerging understanding that complement components can intersect diverse cellular metabolic and effector pathways. Here, the authors propose that the different locations of complement activation dictate its diverse functions.
This Opinion article proposes that higher-order protein complexes — referred to as supramolecular organizing centres (SMOCs) — form on specific organelles by nucleated polymerization downstream of innate immune receptors to amplify the signal and reach a response threshold.
The recent realization that the airways harbour a steady-state microbiota necessitates a shift in our understanding of respiratory health and disease, drawing from similarities with host–microorganism relationships in the intestines.