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  • AIM2 Drives Joint Inflammation in a Self-DNA Triggered Model of Chronic Polyarthritis.

AIM2 Drives Joint Inflammation in a Self-DNA Triggered Model of Chronic Polyarthritis.

PloS one (2015-06-27)
Christopher Jakobs, Sven Perner, Veit Hornung
ABSTRACT

Mice lacking DNase II display a polyarthritis-like disease phenotype that is driven by translocation of self-DNA into the cytoplasm of phagocytic cells, where it is sensed by pattern recognition receptors. While pro-inflammatory gene expression is non-redundantly linked to the presence of STING in these mice, the contribution of the inflammasome pathway has not been explored. To this end, we studied the role of the DNA-sensing inflammasome receptor AIM2 in this self-DNA driven disease model. Arthritis-prone mice lacking AIM2 displayed strongly decreased signs of joint inflammation and associated histopathological findings. This was paralleled with a reduction of caspase-1 activation and pro-inflammatory cytokine production in diseased joints. Interestingly, systemic signs of inflammation that are associated with the lack of DNase II were not dependent on AIM2. Taken together, these data suggest a tissue-specific role for the AIM2 inflammasome as a sensor for endogenous DNA species in the course of a ligand-dependent autoinflammatory condition.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-Viperin Antibody, clone MaP.VIP, clone MaP.VIP, from mouse
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SKUPack SizeAvailabilityPriceQuantity
250 mg
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CA$184.00
Sigma-Aldrich
Nitrogen, ≥99.998%
Sign Into View Organizational & Contract Pricing
SKUPack SizeAvailabilityPriceQuantity
250 mg
Please contact Customer Service for Availability
CA$184.00