Enhanced Th17-cell responses render CCR2-deficient mice more susceptible for autoimmune arthritis.
CCR2 is considered a proinflammatory mediator in many inflammatory diseases such as rheumatoid arthritis. However, mice lacking CCR2 develop exacerbated collagen-induced arthritis. To explore the underlying mechanism, we investigated whether autoimmune-associated Th17 cells were involved in the path...
Main Authors: | , , , , , , , , , , |
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Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2011-01-01
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Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC3186765?pdf=render |