Journal
CELL REPORTS
Volume 9, Issue 5, Pages 1856-1870Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2014.10.067
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Funding
- Cancer Research Institute (CLIP award)
- Ludwig Institute for Cancer Research
- Alliance for Lupus Research
- Melanoma Research Alliance
- Bill and Melinda Gates Foundation
- American Cancer Society
- NIH [R01 AI071078, CCSG 5 P30 CA16087, R37 AI048638, R37 DK057665, U19 AI057266, U19 AI090023]
- NIH/NIAMS [5K99AR062595]
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Matrix metalloproteinase-2 (MMP-2) is involved in several physiological mechanisms, including wound healing and tumor progression. We show that MMP-2 directly stimulates dendritic cells (DCs) to both upregulate OX40L on the cell surface and secrete inflammatory cytokines. The mechanism underlying DC activation includes physical association with Toll-like receptor-2 (TLR2), leading to NF-kappa B activation, OX40L upregulation on DCs, and ensuing TH2 differentiation. Significantly, MMP-2 polarizes T cells toward type 2 responses in vivo, in a TLR2-dependent manner. MMP-2-dependent type 2 polarization may represent a key immune regulatory mechanism for protection against a broad array of disorders, such as inflammatory, infectious, and autoimmune diseases, which can be hijacked by tumors to evade immunity.
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