News & Views |
Featured
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Letter |
Reduction of disulphide bonds unmasks potent antimicrobial activity of human β-defensin 1
This paper shows that the activity of human beta-defensin 1 is regulated by its redox status, with enhanced antibiotic killing activity under reducing conditions as they are found in the distal colon. This is believed to serve to protect the healthy intestinal epithelium against potentially harmful colonization by commensal bacteria and opportunistic fungi. In vitro evidence implicates thioredoxin as the likely reducing agent.
- Bjoern O. Schroeder
- , Zhihong Wu
- & Jan Wehkamp
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Letter |
A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells
Human immunodeficiency virus (HIV) fails to induce interferon in the cells that it infects, but the underlying mechanisms are not known. These authors show that the virus can in fact activate the interferon pathway in dendritic cells when the usual block to infection is bypassed. Dendritic cell activation depends on the HIV-1 capsid/cyclophilin A interaction, which is known to have a role in HIV-1 infectivity.
- Nicolas Manel
- , Brandon Hogstad
- & Dan R. Littman
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News |
Nickel allergy tracked to a single receptor
Molecular pathway reveals why allergen triggers reaction in humans but not in mice.
- Alla Katsnelson
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Outlook |
Learning from the elite
Researchers hope to unlock the secrets of the select few who rein in, or even resist, HIV infection, says Bijal Trivedi.
- Bijal Trivedi
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Letter |
TLR recognition of self nucleic acids hampers glucocorticoid activity in lupus
Glucocorticoids are widely used to treat patients with autoimmune diseases such as systemic lupus erythematosus (SLE), but many treatment regimens cannot maintain disease control in SLE patients. Here it is shown that the stimulation of plasmacytoid dendritic cells through toll-like receptors TLR7 and TLR9 can account for the reduced activity of glucocorticoids to inhibit the type I interferon pathway in SLE patients. Thus inhibitors of TLR7 and TLR9 signalling might prove to be effective corticosteroid-sparing drugs.
- Cristiana Guiducci
- , Mei Gong
- & Franck J. Barrat
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News & Views |
Immunity takes a heavy Toll
Toll receptors trigger immune responses through adaptor proteins and kinase enzymes. Structural studies reveal that hierarchical assembly of these proteins into a helical tower initiates downstream signalling events.
- Steven A. Wasserman
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Letter |
Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity
Here, a new type of innate effector leukocyte cell — the nuocyte — is described and characterized. It is shown that interleukin (IL)25 and IL33 drive the expansion of the nuocyte population, that these cells secrete IL13, and that they are required for protection against helminth infection.
- Daniel R. Neill
- , See Heng Wong
- & Andrew N. J. McKenzie
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Letter |
Circulating mitochondrial DAMPs cause inflammatory responses to injury
Severe trauma can lead to death and sepsis in the absence of apparent infection. Here evidence shows that mitochondrial debris, released from damaged cells, is present in the circulation of seriously injured trauma patients. Such debris is shown to activate neutrophils via specific formyl peptide receptors, triggering systemic inflammation and end organ injury.
- Qin Zhang
- , Mustafa Raoof
- & Carl J. Hauser
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Letter |
An essential role for XBP-1 in host protection against immune activation in C. elegans
The unfolded protein response, known to contribute to the defence against infectious agents and toxins, is shown here to protect Caenorhabditis elegans larvae against detrimental effects of the innate immune response to infection with Pseudomonas aeruginosa. The findings establish innate immunity as a physiologically relevant inducer of ER stress during C. elegans development.
- Claire E. Richardson
- , Tristan Kooistra
- & Dennis H. Kim
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Letter |
FOXO-dependent regulation of innate immune homeostasis
Antimicrobial peptides (AMPs) are an important class of immune effector molecules which fight pathogen infections. AMP induction in Drosophila is regulated through the activation of the Toll and immune deficiency pathways; it is now shown that AMP activation can be achieved independently of these pathways by the transcription factor FOXO. In non-infected animals, AMP genes are activated in response to nuclear FOXO activity when induced by starvation.
- Thomas Becker
- , Gerrit Loch
- & Michael Hoch