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1 tor 1q (C1q) and activation of the classical complement pathway.
2 ants that directly influence the alternative complement pathway.
3 uction, followed by global activation of the complement pathway.
4 s that link glioma pathogenesis with the MBL complement pathway.
5 n ( approximately 65 kDa) is a member of the complement pathway.
6 d C1q and act as inhibitors of the classical complement pathway.
7 to protect Ad5 from attack by the classical complement pathway.
8 d RPE cells, particularly with regard to the complement pathway.
9 bility to normalize activity of the terminal complement pathway.
10 as mediated by natural IgM and the classical complement pathway.
11 mediated by dysregulation of the alternative complement pathway.
12 tients with dysregulation of the alternative complement pathway.
13 ciated with dysregulation of the alternative complement pathway.
14 hese heparinoids can control the alternative complement pathway.
15 t, in part, on activation of the alternative complement pathway.
16 uncontrolled stimulation of the alternative complement pathway.
17 n of a rate-limiting step in the alternative complement pathway.
18 ection, suggesting a defect in the classical complement pathway.
19 suggested an important role for the terminal complement pathway.
20 otic cells, thereby activating the classical complement pathway.
21 (Cfh) is a key regulator of the alternative complement pathway.
22 to C3b signals the start of the alternative complement pathway.
23 erum, an essential component of the terminal complement pathway.
24 livary proteins that inhibit the alternative complement pathway.
25 e lptA mutant occurred through the classical complement pathway.
26 ng therapeutic with selectivity for a single complement pathway.
27 tense genetic and functional analysis of the complement pathway.
28 innate immunity and activator of the lectin complement pathway.
29 ost fluid-phase regulator of the alternative complement pathway.
30 seems to occur primarily via the alternative complement pathway.
31 r H (fH), a key regulator of the alternative complement pathway.
32 riggered activation of C1q and the classical complement pathway.
33 ot of downstream components of the classical complement pathway.
34 I and FcgammaRII and activates the classical complement pathway.
35 ading opsonophagocytosis and the alternative complement pathway.
36 /-), an essential protein in the alternative complement pathway.
37 phils but failed to activate the alternative complement pathway.
38 o contact with components of the alternative complement pathway.
39 initiation of the activation of alternative complement pathway.
40 n-like domain of C1q, a key component in the complement pathway.
41 pivotal C3-convertase, C3bBb, of alternative complement pathway.
42 te to inflammation through activation of the complement pathway.
43 r killing of these targets by activating the complement pathway.
44 alic acid, which inactivates the alternative complement pathway.
45 h IgM indicating activation of the classical complement pathway.
46 omplex dependent activation of the classical complement pathway.
47 the activation and fixation of the classical complement pathway.
48 the dominant Ig and proteins of the classic complement pathway.
49 C1s of the first component of the classical complement pathway.
50 C1q fixation and activation of the classical complement pathway.
51 ericidal activity of NHS via the alternative complement pathway.
52 any components of the classical and terminal complement pathway.
53 in determining appropriate activation of the complement pathway.
54 ecruit natural IgM to initiate the classical complement pathway.
55 ectin protein is the activator of the lectin complement pathway.
56 ich renders them incapable of activating the complement pathway.
57 adhesion of leukocytes and activation of the complement pathway.
58 ating activation of the classical arm of the complement pathway.
59 e classical and lectin (but not alternative) complement pathways.
60 eby inhibiting the classical and alternative complement pathways.
61 to trigger classical as well as alternative complement pathways.
62 ive therapeutics that harness the potency of complement pathways.
63 by inhibiting the classical and alternative complement pathways.
64 on of both the classical and the alternative complement pathways.
65 its both the classical and alternative human complement pathways.
66 that protection by IgG does not require the complement pathways.
67 binds to C3, resulting in suppression of all complement pathways.
68 in both diseases, including inflammasome and complement pathways.
69 Mirolysin exhibited a strong effect on all complement pathways.
70 not saprophytic Leptospira inhibit the three complement pathways.
72 associates with a negative regulator of the complement pathway, a likely mechanism for immune evasio
73 with the recognition proteins of the lectin complement pathway, a recombinant fragment encompassing
74 ruses are potent activators of extracellular complement pathways, a first line of defense that viruse
75 eat inactivation, as well as by the terminal complement pathway Ab eculizumab, the purinergic P2 rece
76 HF1), the major inhibitor of the alternative complement pathway, accumulates within drusen and is syn
77 ement proteins to tubular cells, alternative complement pathway activation and C5b-9-mediated tubular
79 hat C1q induction and classic or alternative complement pathway activation do not contribute signific
83 BL-C, are involved in the Aspergillus-lectin complement pathway activation rather than ficolin-A.
84 red CML and to force a switch from classical complement pathway activation to C1q-dependent alternati
85 Given these results, we conclude that lectin complement pathway activation triggered by ligand-CL-11
88 ccumulating evidence suggests a dysregulated complement pathway among the pathogenic processes of sch
89 olymorphisms (SNPs) in 9 genes in the lectin complement pathway and 3 additional SNPs in MBL2 were te
90 target recognition protein of the classical complement pathway and a major connecting link between i
92 ich may themselves influence the alternative complement pathway and are contained within a common del
93 ne expression of factor B of the alternative complement pathway and C3 in mouse middle ear epithelium
94 OR, 2.17; 95% CI, 1.12-4.24; P = 0.023), the complement pathway and calcified drusen (OR, 3.75; 95% C
95 onnection between the inflammatory classical complement pathway and connective tissue homeostasis.
96 es of ischemic stress, activating the lectin complement pathway and directing the innate immune respo
97 r of innate host immunity that activates the complement pathway and directly opsonises some infectiou
98 q protein, thereby attenuating the classical complement pathway and facilitating pneumococcal complem
99 tein, an opsonic molecule activating classic complement pathway and Fcgamma receptor endocytosis.
100 fluid-phase dysregulation of the alternative complement pathway and frequently deviates from the clas
101 y level, there were associations between the complement pathway and geographic atrophy (GA) (OR, 2.17
102 ry IgM we have investigated the role of each complement pathway and natural IgM for innate immunity t
104 re-establishes regulation of the alternative complement pathway and provide support for a limited tri
105 Uncontrolled activation of the alternative complement pathway and secretion of vascular endothelial
107 ina involves the activity of the alternative complement pathway and that eliminating the alternative
109 proteases required to activate the classical complement pathway, and C3 showed a significant age-depe
110 ent factor H, a regulator of the alternative complement pathway, and LOC387715/HtrA1 are the most con
111 ding to a strong activation of the classical complement pathway, and results in consumption of comple
112 ing CRP-mediated activation of the classical complement pathway, and that the characteristic of CRP t
113 acute-phase response signaling pathway, the complement pathway, and the coagulation pathway are diff
115 activated both the classical and alternative complement pathways, and C1q was found to be crucial for
116 within the PIV5 F protein, the activation of complement pathways, and subsequent complement-mediated
117 to AMR-triggered activation of the classical complement pathway, antibody-dependent cellular cytotoxi
118 at all-trans-retinal (atRal) and alternative complement pathway (AP) activation contribute to RPE cel
120 Uncontrolled activation of the alternative complement pathway (AP) is thought to be associated with
121 irulence, the molecular basis of alternative complement pathway (AP) regulation by meningococcal CPSs
124 As such, selective targeting of pro-allergic complement pathways appears an attractive therapeutic op
125 study was designed to determine which of the complement pathways are activated during acute pneumococ
126 cate that both the classical and alternative complement pathways are critical for middle ear immune d
127 encodes a major inhibitor of the alternative complement pathway, are associated with the risk for dev
128 H (FH), a major regulator of the alternative complement pathway, are associated with various diseases
130 have fully active alternative and classical complement pathways, are protected from cardiac reperfus
131 gene screens have identified members of the complement pathway as contributing to the risk of AMD.
132 zation of activity levels of the alternative complement pathway as measured by C3/C3d ratios and C3Ne
134 g in increased activation of the alternative complement pathway, as a key component of disease biolog
135 xpress and release protein components of the complement pathways, as well as secreting and anchoring
137 ed that cell-bound CL-11 required the lectin complement pathway-associated protease MASP-2 to trigger
138 ypothesized that activation of the classical complement pathway at the endothelial cell surface by HL
139 its serum antibodies that activate classical complement pathway bacteriolysis and also inhibit bindin
141 in eukaryotic cells activated the classical complement pathway but not the alternative or lectin pat
142 alternative (FB(-/-)) or classical (C4(-/-)) complement pathway, but 1A2 was not protective in either
143 Modified forms of LDL activate the classical complement pathway, but no lectin pathway activation was
144 b against C3b that inhibited the alternative complement pathway, but not the classical pathway, was d
145 C activate the classical and the alternative complement pathways, but the role of the lectin pathway
146 Treatment of purified NiV with NHS activated complement pathways, but there was very little C3 deposi
147 factor (DAF; CD55), inhibits the alternative complement pathway by accelerating decay of the converta
148 osylated IgG is related to activation of the complement pathway by mannose-binding lectin, as suggest
149 (FI) is a serine protease that inhibits all complement pathways by degrading activated complement co
150 irst step in the activation of the classical complement pathway, by immune complexes, involves the bi
151 iency of an early component of the classical complement pathway, C1q, C1r/C1s, C4, or C2, regularly p
153 f LTB4 in IC-ALI and activation of C5 by the complement pathway C5 convertase rather than by non-C pr
154 s indicated that activation of the classical complement pathway (CCP) was a primary mechanism for spo
155 ated through activation of each of the three complement pathways (classical, alternative, and lectin)
156 reted proteins involved in regulation of the complement pathway (clusterin, vitronectin, and fibromod
157 both of which encode proteins in the lectin complement pathway (collectin kidney 1 (CL-K1) and MASP-
158 hat genetic variation within early classical complement pathway components (C1q, C1r, and C1s) could
159 hat the alternative pathway was not the only complement pathway contributing to protection against di
164 inopathy (OIR), we observed that alternative complement pathway-deficient mice (Fb(-/-)) exhibited a
166 In contrast, blocking of the alternative complement pathway did not protect this uspA2 mutant fro
168 We investigated the role of the alternative complement pathway during the formation and resolution o
170 C3 plasma values could reflect a more severe complement pathway dysfunction than in AMD, leading to e
171 tivated neutrophils activate the alternative complement pathway, establishing an inflammatory amplifi
172 ether, these findings demonstrate a role for complement pathway factors in fundamental developmental
173 ormal functional properties of the classical complement pathway followed by reduced severity of SLE s
174 sen formation, COL4 accumulation in ECM, and complement pathway gene alteration, it impacted the comp
176 ement component C4 (C4) is a highly variable complement pathway gene situated approximately 500 kb fr
177 of its amplifying property, the alternative complement pathway has been implicated in a number of in
178 racteristic of CRP to activate the classical complement pathway has no role in protecting mice from i
180 early components of the classical and lectin complement pathways have been shown to protect low-densi
181 g lectin gene, a key activator in the lectin complement pathway, have been associated with risk of se
182 nt pathways) or CR2-fH (inhibits alternative complement pathway) immediately posttransplantation.
183 l model that can be used to study the lectin complement pathway in acute and chronic models of human
184 FD) was generated to inhibit the alternative complement pathway in advanced dry age-related macular d
186 To investigate the importance of an intact complement pathway in an experimental staphylococcal inf
189 An enrichment of rare pLoF variants in the complement pathway in cases versus controls (OR, 2.94; 9
190 us, to investigate the role of the classical complement pathway in contusion-induced SCI, male C1q kn
191 ive importance of the Fc receptor versus the complement pathway in disposing antibody-opsonized DAF/C
192 Together, our data implicate the alternative complement pathway in facilitating neovessel clearance b
196 gest a modest involvement of the alternative complement pathway in targeting vessels for regression i
197 st direct genetic evidence for the classical complement pathway in the induction of EAMG induced by A
198 e is known about the role of the alternative complement pathway in the initial vascular regression ph
200 ing further underscores the influence of the complement pathway in the pathogenesis of this disease.
201 Increased activation of the alternative complement pathway in vitreous was controlled by disease
203 CAIA) model, in which the AP is unique among complement pathways in being both necessary and sufficie
204 ential roles of the classical vs alternative complement pathways in EAMG induction, we immunized C3(-
206 tion samples showed upregulation of multiple complement pathways in patients with TMA who had gene va
210 inhibited classical, lectin and alternative complement pathways in vitro when added in excess to hum
213 everal gonococcal strains bind the classical complement pathway inhibitor, C4b-binding protein (C4BP)
214 that lack a major component of the classical complement pathway initiation complex (C1q) but have an
216 r for complement activation, the predominant complement pathway involved, or its role in the pathogen
219 he first step of activation of the classical complement pathway involves the binding of the globular
222 and selective inhibition of the alternative complement pathway is an effective treatment of murine l
227 C1q, the first component of the classical complement pathway, is also a pattern recognition recept
229 The secondary aims were to determine which complement pathways lead to C4d deposition and to determ
230 region of C1q and to initiate the classical complement pathway, leading to activation of C4 and C3,
231 C1q bound to apoptotic cells, activated the complement pathway, leading to C3b deposition, and enhan
236 s a key role in the activation of the lectin-complement pathway of innate immunity, and its deficienc
237 ents kill serum-resistant E. coli though the complement pathway of the innate immune system, suggesti
238 t C4b deposition on live bacteria (classical complement pathway), only those antibodies that inhibite
240 e injection of either CR2-Crry (inhibits all complement pathways) or CR2-fH (inhibits alternative com
241 saline, CR2-fH, CR2-Crry (which inhibits all complement pathways), or soluble CR2 (sCR2; C3d-binding
243 had increased activation of the alternative complement pathway (P = 0.003) and elevated levels of co
244 that requires activation of the alternative complement pathway, passive transfer of antibodies to mo
245 , these data suggest that MBL and the lectin complement pathway play a significant role in vascular d
246 examine recent evidence that the alternative complement pathway plays a key and, in most instances, o
249 of the alternative rather than the classical complement pathway, previously not appreciated for IFTA,
255 g factor H (FH), which is a main alternative complement pathway regulatory protein, have been well ch
256 an however activate the classical and lectin complement pathways, rendering this species still vulner
257 ponse and that activation of the alternative complement pathway represents one of the innate immune d
258 molytic uremic syndrome, blocks the terminal complement pathway required for serum bactericidal activ
261 ) is known to form complexes with the lectin complement pathway serine proteases MASP-1 and MASP-2.
262 gococcal vaccine antigen, activate classical complement pathway serum bactericidal activity (SBA) and
263 C3a complement receptor (C3aR), alternative complement pathway signaling, and antioxidant therapy.
265 bit IgM-mediated activation of the classical complement pathway, since survival of the tspB triple kn
266 by NHS was not due to a global inhibition of complement pathways, since complement was found to signi
267 he absence of both classical and alternative complement pathways suggests that it is the absence of C
268 y disease stage and genetic variation in the complement pathway, supporting a role for complement act
269 e found that despite being recognized by all complement pathways, T. forsythia is resistant to killin
270 ase reflects the activity of the alternative complement pathway that deposits fragments on GBS and th
271 fluid-phase dysregulation of the alternative complement pathway that leads to deposition of complemen
272 he spontaneous activation of the alternative complement pathway that occurs after the genetic absence
273 ity of ficolin-2, an initiator of the lectin complement pathway that was previously shown to bind ST1
274 is a well known inhibitor of the alternative complement pathway, the functions of the CFHR proteins a
275 KE are not associated with activation of the complement pathway, the only other identified cause of t
276 While linked to genetic polymorphisms in the complement pathway, there are many individuals with high
277 self components, and triggers the classical complement pathway through activation of its associated
278 N. gonorrhoeae is mediated by the classical complement pathway through an antibody-dependent mechani
279 ains and to trigger activation of the lectin complement pathway through associated serine proteases.
282 gated BSA triggered activation of the lectin complement pathway, thus further supporting the hypothes
283 phoinositide signalling works in tandem with complement pathways to regulate the activity of Star-PAP
284 prevent complement activation and steer the complement pathway toward generation of inactivated C3b
285 itis result from activation of the classical complement pathway triggered by direct binding of C1q to
286 We found that activation of the classical complement pathway up to C5 was sufficient to neutralize
288 ndicate that ethanol activates the classical complement pathway via C1q binding to apoptotic cells in
289 ata suggest that initiation of the classical complement pathway via C1q is detrimental to recovery af
290 antibodies gain the capacity to activate the complement pathway via mannose-binding lectin (MBL), whi
293 suggesting that activation of the classical complement pathway was not required for innate immunity.
297 e IgM is a potent activator of the classical complement pathway, we examined IgM binding to dying cel
299 variation in a regulator of the alternative complement pathway, when combined with a triggering even
300 an inflammatory cascade via the alternative complement pathway, which is unbridled because the carti
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