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1 rom the bactericidal activity of NHS via the alternative complement pathway.
2 -Ig was more active in inhibiting the murine alternative complement pathway.
3 8 organisms via either the classical or the alternative complement pathway.
4 rabbit erythrocytes due to activation of the alternative complement pathway.
5 ccus neoformans are potent activators of the alternative complement pathway.
6 coding variants that directly influence the alternative complement pathway.
7 rulopathies mediated by dysregulation of the alternative complement pathway.
8 posits in patients with dysregulation of the alternative complement pathway.
9 as been associated with dysregulation of the alternative complement pathway.
10 a result, these heparinoids can control the alternative complement pathway.
11 was dependent, in part, on activation of the alternative complement pathway.
12 is caused by uncontrolled stimulation of the alternative complement pathway.
13 ed inhibition of a rate-limiting step in the alternative complement pathway.
14 ent factor H (Cfh) is a key regulator of the alternative complement pathway.
15 vation of C3 to C3b signals the start of the alternative complement pathway.
16 y of tick salivary proteins that inhibit the alternative complement pathway.
17 actor H, a host fluid-phase regulator of the alternative complement pathway.
18 usion (I/R) seems to occur primarily via the alternative complement pathway.
19 binds factor H (fH), a key regulator of the alternative complement pathway.
20 means of evading opsonophagocytosis and the alternative complement pathway.
21 actor B (fB-/-), an essential protein in the alternative complement pathway.
22 human neutrophils but failed to activate the alternative complement pathway.
23 ri comes into contact with components of the alternative complement pathway.
24 ible for the initiation of the activation of alternative complement pathway.
25 to form the pivotal C3-convertase, C3bBb, of alternative complement pathway.
26 ated with sialic acid, which inactivates the alternative complement pathway.
27 1 inhibitor (C1-INH) as an inhibitor of the alternative complement pathway.
28 da albicans activates both the classical and alternative complement pathways.
29 affected killing through both classical and alternative complement pathways.
30 yeast and contributions of the classical and alternative complement pathways.
31 tein C, thereby inhibiting the classical and alternative complement pathways.
32 is required to trigger classical as well as alternative complement pathways.
33 iated injury by inhibiting the classical and alternative complement pathways.
34 tes activation of both the classical and the alternative complement pathways.
35 regulates the activity of both classical and alternative complement pathways.
36 eposition on the yeast via the classical and alternative complement pathways.
37 and C4 of the classical and lectin (but not alternative) complement pathways.
38 TNFSF13 locus, 22q12 HORMAD2 locus), and the alternative complement pathway (1q32 CFH/CFHR locus).
39 t factor H (HF1), the major inhibitor of the alternative complement pathway, accumulates within druse
41 vating complement proteins to tubular cells, alternative complement pathway activation and C5b-9-medi
42 tablishing that C1q induction and classic or alternative complement pathway activation do not contrib
44 l classical complement pathway and show that alternative complement pathway activation is an importan
46 ytotoxic antibodies as well as classical and alternative complement pathway activities were determine
47 essed classical complement pathway activity, alternative complement pathway activity, and the C3 comp
48 era from Bf-deficient mice lacked detectable alternative complement pathway activity; purified mouse
49 nd CFHR1, which may themselves influence the alternative complement pathway and are contained within
50 increased gene expression of factor B of the alternative complement pathway and C3 in mouse middle ea
51 sera neutralized virus, suggesting that the alternative complement pathway and complement components
52 s caused by fluid-phase dysregulation of the alternative complement pathway and frequently deviates f
53 soluble CR1 re-establishes regulation of the alternative complement pathway and provide support for a
55 -damaged retina involves the activity of the alternative complement pathway and that eliminating the
56 that complement factor H, a regulator of the alternative complement pathway, and LOC387715/HtrA1 are
57 ibe that CC activated both the classical and alternative complement pathways, and C1q was found to be
58 suggests that all-trans-retinal (atRal) and alternative complement pathway (AP) activation contribut
61 ingococcal virulence, the molecular basis of alternative complement pathway (AP) regulation by mening
64 indings indicate that both the classical and alternative complement pathways are critical for middle
65 HF1), which encodes a major inhibitor of the alternative complement pathway, are associated with the
66 ting factor H (FH), a major regulator of the alternative complement pathway, are associated with vari
67 d be normalization of activity levels of the alternative complement pathway as measured by C3/C3d rat
68 ides directly and independently activate the alternative complement pathway as well as the classical
69 H, resulting in increased activation of the alternative complement pathway, as a key component of di
71 A phage Ab against C3b that inhibited the alternative complement pathway, but not the classical pa
73 ccelerating factor (DAF; CD55), inhibits the alternative complement pathway by accelerating decay of
76 -induced retinopathy (OIR), we observed that alternative complement pathway-deficient mice (Fb(-/-))
77 ase-associated CFH genetic variants had more alternative complement pathway deposits than controls.
81 nabling the bacteria to avoid killing by the alternative complement pathway during vertebrate infecti
83 By virtue of its amplifying property, the alternative complement pathway has been implicated in a
84 ormally dampens the activation of C3 via the alternative complement pathway, has been seen in some pa
85 all complement pathways) or CR2-fH (inhibits alternative complement pathway) immediately posttranspla
86 fragment (AFD) was generated to inhibit the alternative complement pathway in advanced dry age-relat
91 our data suggest a modest involvement of the alternative complement pathway in targeting vessels for
92 wever, little is known about the role of the alternative complement pathway in the initial vascular r
93 antigen processing and presentation, and the alternative complement pathway in the pathogenesis of Ig
95 was shown to be a selective inhibitor of the alternative complement pathway in vitro and to function
96 e the differential roles of the classical vs alternative complement pathways in EAMG induction, we im
97 cells and shown to inhibit the classical and alternative complement pathways in vitro and in vivo.
98 uman IalphaI inhibited classical, lectin and alternative complement pathways in vitro when added in e
101 Targeted and selective inhibition of the alternative complement pathway is an effective treatment
102 Candida albicans activates the classical and alternative complement pathways, leading to deposition o
103 tal systems, to be capable of activating the alternative complement pathway, making IgA antibodies po
105 AMD patients had increased activation of the alternative complement pathway (P = 0.003) and elevated
106 In a manner that requires activation of the alternative complement pathway, passive transfer of anti
107 Herein we examine recent evidence that the alternative complement pathway plays a key and, in most
114 ies targeting factor H (FH), which is a main alternative complement pathway regulatory protein, have
115 e immune response and that activation of the alternative complement pathway represents one of the inn
116 by blocking C3a complement receptor (C3aR), alternative complement pathway signaling, and antioxidan
117 ere SLE in the absence of both classical and alternative complement pathways suggests that it is the
118 re factor H, a critical downregulator of the alternative complement pathway, than their Por1B counter
119 F-alpha release reflects the activity of the alternative complement pathway that deposits fragments o
120 cterized by fluid-phase dysregulation of the alternative complement pathway that leads to deposition
121 ccount for the spontaneous activation of the alternative complement pathway that occurs after the gen
122 gh factor H is a well known inhibitor of the alternative complement pathway, the functions of the CFH
123 assayed for inhibition of the classical and alternative complement pathways using standard CH(50) an
124 that genetic variation in a regulator of the alternative complement pathway, when combined with a tri
125 ces initiate an inflammatory cascade via the alternative complement pathway, which is unbridled becau
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