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In this Opinion article, the authors propose that the immunological process that underlies type 1 diabetes is relapsing–remitting in nature; they highlight the supporting evidence and the remaining controversies, and discuss the possible therapeutic implications of their hypothesis.
Here, the authors propose a new mechanism of immune tolerance. It involves the production of the immunoregulatory enzyme IDO (indoleamine 2,3-dioxygenase) induced by reverse signalling and non-canonical nuclear factor-κB activation in dendritic cells interacting with regulatory-T-cell-expressed co-receptors.
The activating receptor NKG2D (natural-killer group 2, member D) recognizes an array of ligands that are upregulated by cellular stress. But what value is it for the host to express so many ligands for one receptor, and what drives NKG2D-ligand diversity?
What is immune computing? Can the immune system compute? Does it use a computational strategy to function? In this Opinion article, Irun Cohen proposes that the answer to these questions is yes, and applies these ideas to different types of immunity.
A number of different non-conventional T-cell lineages with innate phenotypes have been identified. As outlined here, it seems likely that 'innate' T cells develop as a result of interactions with non-classical MHC molecules expressed by haematopoietic cells in the thymus.
The DRiP hypothesis proposes that most peptides that bind to MHC class I molecules are derived from newly synthesized defective proteins. Here, the authors revise this hypothesis and propose that some peptides result from the random delivery of unchaperoned nascent polypeptides to the proteasome.
The success and pathogenicity of HIV-1 largely resides in the function of the viral protein Nef. Here, the authors propose that Nef modulates a T cell's ability to form an immunological synapse and modulates T-cell activation to favour viral replication and spread.
The transcription factor forkhead box P3 (FOXP3) is essential for the development and function of regulatory T cells. Here, the authors propose that FOXP3 might also influence how a cell responds to T-cell receptor stimulation and what tissue-homing receptors it expresses.
How can your thymus continue to generate the necessary numbers of CD4+CD25+ regulatory T (TReg) cells once it involutes? Arne Akbar and colleagues propose a model whereby some TRegcells differentiate from rapidly proliferating memory T cells in the periphery.
The intercellular transfer of cell-surface proteins is known to occur between immune cells, but how common is this occurrence, what are its mechanisms and is it important in influencing the interactions of immune cells?
The immune-system–brain interface is a crucial route for communication between the brain in health and disease and environmental pathogens and toxins. Can systemic infections and inflammation associated with chronic neurodegenerative diseases exacerbate symptoms and drive the progression of neurodegeneration?
Although the only signalling motif in the adaptor protein DAP12 is generally thought to transduce activating signals, DAP12 has recently been shown to have inhibitory effects. A model to explain how this might occur is proposed in this Opinion article.
Translating basic research into viable therapies is challenged by many obstacles. In this Opinion article, Ian Sabroe and colleagues identify some of these obstacles and suggest a series of strategies to maximize the potential of translational research.