In this section
@article{Ruseva:2014:10.1111/cei.12244,
author = {Ruseva, MM and Takahashi, M and Fujita, T and Pickering, MC},
doi = {10.1111/cei.12244},
journal = {Clinical and Experimental Immunology},
pages = {84--92},
title = {C3 dysregulation due to factor H deficiency is mannan-binding lectin-associated serine proteases (MASP)-1 and MASP-3 independent in vivo},
url = {http://dx.doi.org/10.1111/cei.12244},
volume = {176},
year = {2014}
}
TY - JOUR
AB - Uncontrolled activation of the complement alternative pathway is associated with complementmediated renal disease. Factor B and factor D are essential components of this pathway, while factor H (FH) is its major regulator. In complete FH deficiency, uncontrolled C3 activation through the alternative pathway results in plasma C3 depletion and complementmediated renal disease. These are dependent on factor B. Mannanbinding lectinassociated serine proteases 1 and 3 (MASP1, MASP3) have been shown recently to contribute to alternative pathway activation by cleaving profactor D to its active form, factor D. We studied the contribution of MASP1 and MASP3 to uncontrolled alternative pathway activation in experimental complete FH deficiency. Codeficiency of FH and MASP1/MASP3 did not ameliorate either the plasma C3 activation or glomerular C3 accumulation in FHdeficient mice. Our data indicate that MASP1 and MASP3 are not essential for alternative pathway activation in complete FH deficiency.
AU - Ruseva,MM
AU - Takahashi,M
AU - Fujita,T
AU - Pickering,MC
DO - 10.1111/cei.12244
EP - 92
PY - 2014///
SN - 0009-9104
SP - 84
TI - C3 dysregulation due to factor H deficiency is mannan-binding lectin-associated serine proteases (MASP)-1 and MASP-3 independent in vivo
T2 - Clinical and Experimental Immunology
UR - http://dx.doi.org/10.1111/cei.12244
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000332307300009&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - https://onlinelibrary.wiley.com/doi/10.1111/cei.12244
VL - 176
ER -