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Recent research on MALT1 (mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1), a protein essential for nuclear factor-κB (NF-κB) activation, has uncovered new mechanisms by which MALT1 can orchestrate intracellular signalling events. Here, Margot Thome highlights recent progress which characterizes how the protease and scaffolding functions of MALT1 modulate T-cell activation.
This Review describes the significant progress that has been made recently in our understanding of the immunoregulatory role of deubiquitylation. Shao-Cong Sun discusses the deubiquitylating enzymes, in particular CYLD and A20, that have been shown to modulate innate and adaptive immunity.
A decline in T-cell immunity is a major cause of morbidity and mortality from infectious diseases in the elderly. Janko Nikolich-Žugich weighs up the relative roles of and the interplay between homeostatic factors and persistent viruses in immune senescence.
Regulatory T cells (TReg cells) have a central role in immune regulation, but how do they work? In this Review, our current understanding of the suppressive mechanisms used by TReg cells is described and the relative contribution of these mechanisms to TReg-cell function is discussed.
As discussed in this article, in addition to their role as haematopoietic-cell growth factors, colony-stimulating factors have broader roles in immunity, and targeting these factors might have therapeutic benefits in inflammation and autoimmunity.
Surprisingly, and somewhat counter-intuitively, partial T-cell immunodeficiencies are commonly associated with hyper-immune dysregulation. Here, the authors review the genetic basis of such immunodeficiencies and draw on mouse models to provide a potential explanation for the coexistence of immunodeficiency and autoimmunity.
Type I interferons (IFNs) provide the first line of defence against viral infection. As discussed in this Review, the IFN-induced antiviral effector proteins, such as ISG15, Mx proteins, ribonuclease L and protein kinase R, are important components of this response.
