Skip to main content
. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: J Immunol. 2017 Jul 24;199(5):1835–1845. doi: 10.4049/jimmunol.1700119

FIGURE 7.

FIGURE 7

A putative LP-AP pathway model to trigger arthritis using the LP ligand and enzymes to activate the AP. Here we show how FCN B, MASP-1 and MASP-2 may act in concert or independently to trigger AP pathway to induce CAIA. This model regarding the role of FCNs and MASP-2 is based on the finding that both mice lacking FCN B and MASP-2 were partially protected from CAIA. FCN B could be the major ligand in mouse to activate the AP via LP by binding to MASP-1 and activating the C3 directly or directly activating the AP by binding to MASP-3. MASP-2 definitely can cause activation of the AP via C4-independent pathway. Blue and red dotted arrows show possible activation routes to activate the AP and the AP amplification loop.