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1 le (non-hemolytic, and poor activator of the complement system).
2 eceptors TLR-2 and TLR-4, FcgammaRs, and the complement system).
3 h respect to regulators and receptors of the complement system.
4 ities in the alternative pathway (AP) of the complement system.
5 of the three main activation cascades of the complement system.
6 the classical and lectin pathways within the complement system.
7 regulation of the alternative pathway of the complement system.
8 the activation and effector functions of the complement system.
9 o self versus non-self discrimination by the complement system.
10 hology by their capacity to overactivate the complement system.
11 ic circulation through the regulation of the complement system.
12 se, including the bactericidal effect of the complement system.
13 ve evolved multiple strategies to escape the complement system.
14 sist the antimicrobial activity of the human complement system.
15 Activated platelets can activate the complement system.
16 ble to malignancy through proteolysis of the complement system.
17 his was independent on the activation of the complement system.
18 d injury and, possibly, the evolution of the complement system.
19 PPARalpha and TNFalpha in the regulation of complement system.
20 several strategies to evade detection by the complement system.
21 e implicated an interaction of Trx1 with the complement system.
22 f the central regulatory component C3 of the complement system.
23 mers is critical to evade recognition by the complement system.
24 ere they may interact with components of the complement system.
25 . enterocolitica effectively evades the host complement system.
26 y proteins of the alternative pathway of the complement system.
27 Ps are activated, which in turn activate the complement system.
28 and protection was dependent upon an active complement system.
29 isticated array of proteins that inhibit the complement system.
30 ein (VCP), respectively, to subvert the host complement system.
31 ere, we report a novel role for CFHR4 in the complement system.
32 regulator of the alternative pathway of the complement system.
33 antibody-independent activation route of the complement system.
34 nd protects the pathogen from killing by the complement system.
35 well-established activation pathways of the complement system.
36 of therapeutic approaches that modulate the complement system.
37 pattern- recognition receptors (PRRs) of the complement system.
38 activation of the alternative pathway of the complement system.
39 ocally overcome systemic inactivation by the complement system.
40 otect themselves against killing by the host complement system.
41 plex relationship between merozoites and the complement system.
42 ay and triggers the kallikrein-kinin and the complement systems.
43 concurrently activates both coagulation and complement systems.
44 complex (TCC) is formed on activation of the complement system, a crucial arm of innate immunity.
47 -3) is a member of the lectin pathway of the complement system, a key component of human innate and a
49 dy provides mechanistic insight into how the complement system, a key component of innate immunity, r
54 Recent investigations demonstrated that the complement system activation participates in 2 critical
55 y antiphospholipid antibodies and subsequent complement system activation play a cardinal role in APS
56 tonomous neuroinflammatory response, classic complement system activation, and STAT3 activation throu
57 It has been recently demonstrated that the complement system activation, which is one of the first
65 an serum because they successfully evade the complement system, an important arm of innate immunity.
69 ell as the MASP SP inhibit the action of the complement system and also show a significant associatio
71 on represents a novel connection between the complement system and cell surface PDI-mediated thiol-di
72 actor H-related protein 2 (CFHR2, related to complement system and coagulant mechanism) were selected
75 factor H (CFH) is a central regulator of the complement system and has been implicated in the etiolog
76 e data establish a critical link between the complement system and immunometabolic adaptations drivin
77 appears to be involved in activation of the complement system and in the production of chemotactic a
79 comprised the first element of the original complement system and initially functioned intracellular
80 mune response to self-antigens activates the complement system and initiates the inflammatory cascade
81 n activation pattern involving the classical complement system and its associated phagosome pathway.
82 ior research has established the role of the complement system and its effector proteins in the progr
87 ms are poorly understood, roles for both the complement system and reactive macrophages have been imp
88 les exhibited particular upregulation of the complement system and respective regulatory pathways, wi
90 oteases, activates the lectin pathway of the complement system and subsequent inflammatory mechanisms
92 mplex crosstalk between the endothelium, the complement system and the hemostasis in health and in di
93 ional connections between alterations in the complement system and the pathogenesis of MD remain to b
95 m, causing activation of the coagulation and complement systems and clearance of transplanted cells.
96 ry protein in the alternative pathway of the complement system, and CFH polymorphisms increase the ge
97 R signaling cross-talks extensively with the complement system, and combined CD14 and complement inhi
98 CRPs prevent attack on host cells by the complement system, and complement receptor 1-like protei
99 broad link between the kinin-kallikrein and complement systems, and suggest a role of CPN1 in the co
100 scripts sensitive to infection and implicate complement system, antigen processing and presentation,
101 The classical and lectin pathways of the complement system are important for the elimination of p
103 4 and Ptx3, in addition to activation of the complement system, as measured by immune cell infiltrati
104 in certain anti-proteases and in the immune complement system, both of which react with the ligand o
105 tion or development systemically inhibit the complement system, but since complement is important for
109 ing evidence suggests that components of the complement system, C1q and C3, can mediate elimination o
110 s involved in bacterial killing, such as the complement system, can also exert cytolytic activity aga
112 P. ovis infestation, including roles for the complement system, clotting cascade and fibrinolysis.
124 te that blockade of TLR4, P-selectin, or the complement system could prevent liver injury in hemolyti
125 les, such as Toll-like receptors (TLRs), the complement system, cytokines, chemokines, inflammatory r
126 As FH is responsible for regulating the complement system, decreased affinity for heparin result
127 n C3 (C3(-/-)), an upstream component of the complement system, did not affect mouse susceptibility t
129 and compelling insight into the role of the complement system during mammalian embryonic development
130 this study, we have examined the role of the complement system during the priming phase of liver rege
131 une system is a central player, in which the complement system emerges as a pivotal part of liver hom
134 anized sialome (Cmah(-/-) mice) or humanized complement system (FH/C4b-binding protein transgenic mic
136 data was performed to analyze variants in 32 complement system genes for positive association with CA
137 nly associated with rare genetic variants in complement system genes, unique to each patient/family.
144 mmunological and inflammatory processes, the complement system has emerged as an attractive target fo
151 lar degeneration (AMD), rare variants in the complement system have been described, but their functio
154 n of redox homeostasis and activation of the complement system, immune cell infiltration, and phagocy
156 les include ADEVs spreading the dysregulated complement system in AD, mediating motoneuron toxicity i
157 regulates the terminal pathway of the human complement system in addition to being a component of th
160 Cumulative evidence indicates a role for the complement system in both pathology and recovery after i
162 ains, indicating the importance of an intact complement system in clearing Pseudomonas infection duri
163 mportance of C5a and other components of the complement system in inflammatory and neuropathic pain,
167 etermined the impact of HIV infection on the complement system in patients with asymptomatic HIV infe
170 dy, we address the involvement of NA and the complement system in the activation of innate immunity t
172 study we established the involvement of the complement system in the recognition and the phagocytosi
175 a potent modulator of the blood clotting and complement systems in hemostasis, thrombosis, and inflam
176 ical matter for this pivotal protease of the complement system: in silico active site mapping for hot
177 lation, has led to the appreciation that the complement system includes membrane inhibitors that are
178 n to possess several mechanisms to evade the complement system, including binding to complement inhib
179 ria employ a variety of tactics to evade the complement system, including recruitment of complement r
188 ing inflammation including activation of the complement system is a hallmark of systemic lupus erythe
194 asome caspase-1 activation, showing that the complement system is a key trigger in CC-induced inflamm
217 The membrane attack complex (MAC) of the complement system is detected in the traumatized brain e
233 regulator of the alternative pathway of the complement system, is only expressed in the eye and on t
234 ng substances and subsequently activates the complement system, it has been proposed that the antipne
236 by genetic and acquired abnormalities of the complement system leading to alternative pathway (AP) ov
237 empt to evade annihilation by the vertebrate complement system, many microbes capture factor H (FH),
238 nt studies have shown that activation of the complement system may be associated with long-term graft
239 regeneration, and suggest that manipulating complement system may produce therapeutic benefit in mus
243 n through opsonization and activation of the complement system on surfaces with an appropriate presen
244 e identified metabolites and activity of the complement system, one of the main AMD-associated diseas
245 of plaque-induced genes (PIGs) involving the complement system, oxidative stress, lysosomes, and infl
251 The coordinated activity between MCs and the complement system plays a key role, for example, in a nu
253 et al. is one such team who report that the complement system plays a substantial role in creating t
258 Interactions between T helper cells and the complement system promote loss of sensory neurons in the
260 ckout mice with concomitant normalization of complement system protein expression and reduction of bi
261 force microscopy (AFM), here we studied two complement system proteins at the single-molecule level:
262 nalysis revealed the presence of Igs and the complement system proteins C3, factor B, and clusterin.
265 uctural and mechanistic understanding of the complement system rationalizes the genetic defects confe
266 versely, only E coli challenge activated the complement system, reaching a maximum at 2 hours postcha
267 its ligand C3d provides insight into how the complement system regulates access of antigen by B cells
270 ts show that therapeutic manipulation of the complement system requires rigorous disease-specific tar
272 mplement component C4 upon activation of the complement system's classical and lectin pathways, which
274 activation of the alternative pathway of the complement system strongly contributes to serum MMP-8 co
275 ociated with an inadequate regulation of the complement system, supporting current evidence on the ro
276 C1q, the initiating component of the classic complement system that is the protein-based arm of the i
278 , the discovery of an intracellularly active complement system-the complosome-and its key role in the
279 ding antigen-specific IA interferes with the complement system; this effect may be partially responsi
280 ovel mechanism by which NiV evades the human complement system through a unique factor I-like activit
281 subjected to repeated exposures to the host complement system through cyclic infections of mammalian
282 study we hypothesized whether CC employ the complement system to activate inflammasome/caspase-1, le
286 d brain disorders.SIGNIFICANCE STATEMENT The complement system, traditionally known as a controller o
288 ogrammer of cell metabolism suggest that the complement system utilizes C3 to guard not only extracel
291 ta-fibrils in Alzheimer disease activate the complement system, we have here investigated specific in
292 respectively) while acute phase response and complement system were affected stronger in Cbs(-/-) mic
293 including acute-phase response signaling and complement system) were overexpressed in the follicular
296 indings provide initial evidence linking the complement system with cortical thinning in humans, a pr
297 During sepsis, excessive activation of the complement system with generation of the anaphylatoxin C
298 ial sepsis triggers robust activation of the complement system with subsequent generation of anaphyla
299 lly, we investigated activation of the local complement system within the dental pulp and its role in
300 these results suggest that IgM activates the complement system within the glomerulus in an animal mod