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Antimicrobial proteins are an ancient mechanism of defence against pathogens at skin and mucosal surfaces. As discussed in this Progress article, new studies identify dynamic cross-regulation between cytokines and antimicrobial peptides, which contributes to immunity and homeostasis at these sites.
Activation of nuclear factor-κB (NF-κB) is crucial for initiating inflammatory responses. In this Review, Sankar Ghosh and Matthew Hayden discuss the roles of several newly identified regulators of the NF-κB pathway, as well as some old factors that have been assigned new functions.
The tripartite motif-containing (TRIM) proteins are best known for their roles in the restriction of infection by lentiviruses. Here, the authors describe the recent studies that reveal broader antiviral and antimicrobial activities of TRIM proteins, including an involvement in the pathogen-recognition and signalling pathways.
Herpesviruses have evolved numerous strategies to outsmart the host and establish persistent infection. Important targets of viral entry and immunomodulation are the tumour-necrosis factor superfamily proteins. This Review describes the central role of these proteins in both virus survival and host defence.
This Review discusses how the diversity of glycan structures that are produced in the secretory pathway and are displayed at the cell surface and in extracellular compartments can have both homeostatic and pathogenic effects on the development and function of the mammalian immune system.
These authors express their opinion that we should devote more research attention to uncovering the mechanisms by which a host can tolerate, as well as resist, infection with a pathogen. New drugs to increase tolerance to infection should provide therapies to which pathogens will not develop resistance.
This article proposes that endogenous peptides can enhance the recognition of antigenic peptides by T cells and, based on results from MHC class I- and class II-restricted T-cell systems, that CD4 and CD8 have different roles in the recognition of endogenous peptide–MHC complexes.
