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1 eceptors TLR-2 and TLR-4, FcgammaRs, and the complement system).
2 le (non-hemolytic, and poor activator of the complement system).
3 regulation of the alternative pathway of the complement system.
4 the activation and effector functions of the complement system.
5 o self versus non-self discrimination by the complement system.
6 hology by their capacity to overactivate the complement system.
7 ic circulation through the regulation of the complement system.
8 se, including the bactericidal effect of the complement system.
9 ve evolved multiple strategies to escape the complement system.
10 sist the antimicrobial activity of the human complement system.
11 Activated platelets can activate the complement system.
12 ble to malignancy through proteolysis of the complement system.
13 his was independent on the activation of the complement system.
14 PPARalpha and TNFalpha in the regulation of complement system.
15 several strategies to evade detection by the complement system.
16 e implicated an interaction of Trx1 with the complement system.
17 f the central regulatory component C3 of the complement system.
18 mers is critical to evade recognition by the complement system.
19 ere they may interact with components of the complement system.
20 . enterocolitica effectively evades the host complement system.
21 y proteins of the alternative pathway of the complement system.
22 Ps are activated, which in turn activate the complement system.
23 and protection was dependent upon an active complement system.
24 isticated array of proteins that inhibit the complement system.
25 ein (VCP), respectively, to subvert the host complement system.
26 ere, we report a novel role for CFHR4 in the complement system.
27 antibody-independent activation route of the complement system.
28 nd protects the pathogen from killing by the complement system.
29 well-established activation pathways of the complement system.
30 teases involved in blood coagulation and the complement system.
31 lular functions and include among others the complement system.
32 release of IL-17F and its regulation by the complement system.
33 as an opsonin and through activation of the complement system.
34 to the resultant renal injury, including the complement system.
35 plex relationship between merozoites and the complement system.
36 neurodegeneration, this study focused on the complement system.
37 influence recognition of C. albicans by the complement system.
38 at SV5 may have mechanisms to evade the host complement system.
39 eptors on effector cells, in addition to the complement system.
40 ss virulence factors that inhibit the host's complement system.
41 ein being responsible for homeostasis of the complement system.
42 e evasion proteins, many of which target the complement system.
43 oniae and subsequent activation of the mouse complement system.
44 h respect to regulators and receptors of the complement system.
45 ities in the alternative pathway (AP) of the complement system.
46 of the three main activation cascades of the complement system.
47 the classical and lectin pathways within the complement system.
48 concurrently activates both coagulation and complement systems.
49 ion of the inflammatory kallikrein-kinin and complement systems.
50 ay and triggers the kallikrein-kinin and the complement systems.
52 ly the viral coat protein (CP), suppress the complement system, a fundamental component of the innate
53 -3) is a member of the lectin pathway of the complement system, a key component of human innate and a
55 dy provides mechanistic insight into how the complement system, a key component of innate immunity, r
59 y antiphospholipid antibodies and subsequent complement system activation play a cardinal role in APS
60 tonomous neuroinflammatory response, classic complement system activation, and STAT3 activation throu
61 It has been recently demonstrated that the complement system activation, which is one of the first
67 ruption of the central component (C3) of the complement system ameliorated muscle pathology in dysfer
68 an serum because they successfully evade the complement system, an important arm of innate immunity.
73 nt factor C3 is the central component of the complement system and a key inflammatory protein activat
75 ell as the MASP SP inhibit the action of the complement system and also show a significant associatio
77 on represents a novel connection between the complement system and cell surface PDI-mediated thiol-di
78 actor H-related protein 2 (CFHR2, related to complement system and coagulant mechanism) were selected
80 acterized by intravascular activation of the complement system and deposition of complement fragments
82 factor H (CFH) is a central regulator of the complement system and has been implicated in the etiolog
83 e data establish a critical link between the complement system and immunometabolic adaptations drivin
84 appears to be involved in activation of the complement system and in the production of chemotactic a
86 comprised the first element of the original complement system and initially functioned intracellular
87 mune response to self-antigens activates the complement system and initiates the inflammatory cascade
88 n activation pattern involving the classical complement system and its associated phagosome pathway.
89 ior research has established the role of the complement system and its effector proteins in the progr
92 f FDC function and suggest new ways that the complement system and persistent antigen presentation mi
93 ms are poorly understood, roles for both the complement system and reactive macrophages have been imp
94 les exhibited particular upregulation of the complement system and respective regulatory pathways, wi
96 oteases, activates the lectin pathway of the complement system and subsequent inflammatory mechanisms
98 indings explain the interactions between the complement system and T cells that are critical for the
99 mplex crosstalk between the endothelium, the complement system and the hemostasis in health and in di
100 ional connections between alterations in the complement system and the pathogenesis of MD remain to b
102 ry protein in the alternative pathway of the complement system, and CFH polymorphisms increase the ge
103 R signaling cross-talks extensively with the complement system, and combined CD14 and complement inhi
104 CRPs prevent attack on host cells by the complement system, and complement receptor 1-like protei
105 broad link between the kinin-kallikrein and complement systems, and suggest a role of CPN1 in the co
106 scripts sensitive to infection and implicate complement system, antigen processing and presentation,
108 4 and Ptx3, in addition to activation of the complement system, as measured by immune cell infiltrati
109 in certain anti-proteases and in the immune complement system, both of which react with the ligand o
110 tion or development systemically inhibit the complement system, but since complement is important for
114 ing evidence suggests that components of the complement system, C1q and C3, can mediate elimination o
115 m the cleavage of the third component of the complement system (C3), is evidence for activation of co
116 s involved in bacterial killing, such as the complement system, can also exert cytolytic activity aga
117 injection, the intraocular activation of the complement system caused induction and progression of CN
119 P. ovis infestation, including roles for the complement system, clotting cascade and fibrinolysis.
129 les, such as Toll-like receptors (TLRs), the complement system, cytokines, chemokines, inflammatory r
130 n C3 (C3(-/-)), an upstream component of the complement system, did not affect mouse susceptibility t
132 and compelling insight into the role of the complement system during mammalian embryonic development
133 this study, we have examined the role of the complement system during the priming phase of liver rege
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.
140 ation in genes involved in regulation of the complement system has been implicated as a major cause o
143 nce between activation and inhibition of the complement system has been implicated in the etiologies
147 mmunological and inflammatory processes, the complement system has emerged as an attractive target fo
154 lar degeneration (AMD), rare variants in the complement system have been described, but their functio
157 regulates the terminal pathway of the human complement system in addition to being a component of th
160 ment activation, the functional roles of the complement system in atherogenesis are not yet fully res
161 Cumulative evidence indicates a role for the complement system in both pathology and recovery after i
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
169 dy, we address the involvement of NA and the complement system in the activation of innate immunity t
172 identify a central role for the inflammatory complement system in the pathogenesis of osteoarthritis.
173 The identification of involvement of the complement system in the pathophysiology of AAA provides
174 though studies have suggested a role for the complement system in the pathophysiology of spinal cord
175 study we established the involvement of the complement system in the recognition and the phagocytosi
177 a potent modulator of the blood clotting and complement systems in hemostasis, thrombosis, and inflam
178 ical matter for this pivotal protease of the complement system: in silico active site mapping for hot
179 lation, has led to the appreciation that the complement system includes membrane inhibitors that are
180 n to possess several mechanisms to evade the complement system, including binding to complement inhib
181 ease model in which genetic variation in the complement system increases the risk of AMD by a combina
187 ing inflammation including activation of the complement system is a hallmark of systemic lupus erythe
192 asome caspase-1 activation, showing that the complement system is a key trigger in CC-induced inflamm
193 is that recognition of tubular injury by the complement system is a major mechanism by which the syst
211 The membrane attack complex (MAC) of the complement system is detected in the traumatized brain e
226 regulator of the alternative pathway of the complement system, is only expressed in the eye and on t
227 ng substances and subsequently activates the complement system, it has been proposed that the antipne
230 by genetic and acquired abnormalities of the complement system leading to alternative pathway (AP) ov
231 nal proposal by Fearon and Locksley that the complement system linked innate and adaptive immunity, t
232 empt to evade annihilation by the vertebrate complement system, many microbes capture factor H (FH),
233 by anti-BP180 antibodies and depends on the complement system, mast cell (MC) degranulation, and neu
234 nt studies have shown that activation of the complement system may be associated with long-term graft
235 regeneration, and suggest that manipulating complement system may produce therapeutic benefit in mus
237 sferlinopathy and suggest that targeting the complement system might serve as a therapeutic approach
238 hesis of C1q, a recognition component of the complement system, occurs in brain during ischemia/reper
240 n through opsonization and activation of the complement system on surfaces with an appropriate presen
256 proinflammatory cytokines, activation of the complement system, production of autoantibodies, overexp
258 nalysis revealed the presence of Igs and the complement system proteins C3, factor B, and clusterin.
259 eriments with human and mouse phagocytes and complement systems provide additional evidence to suppor
261 uctural and mechanistic understanding of the complement system rationalizes the genetic defects confe
262 versely, only E coli challenge activated the complement system, reaching a maximum at 2 hours postcha
263 its ligand C3d provides insight into how the complement system regulates access of antigen by B cells
265 ts show that therapeutic manipulation of the complement system requires rigorous disease-specific tar
267 mplement component C4 upon activation of the complement system's classical and lectin pathways, which
270 activation of the alternative pathway of the complement system strongly contributes to serum MMP-8 co
271 ociated with an inadequate regulation of the complement system, supporting current evidence on the ro
272 C1q, the initiating component of the classic complement system that is the protein-based arm of the i
273 onal gene networks, including members of the complement system, that appeared to be related to cIOPx,
275 ding antigen-specific IA interferes with the complement system; this effect may be partially responsi
276 ovel mechanism by which NiV evades the human complement system through a unique factor I-like activit
277 subjected to repeated exposures to the host complement system through cyclic infections of mammalian
278 study we hypothesized whether CC employ the complement system to activate inflammasome/caspase-1, le
283 d brain disorders.SIGNIFICANCE STATEMENT The complement system, traditionally known as a controller o
285 h to examine the interaction of NPs with the complement system using in vitro assays and correlating
286 ogrammer of cell metabolism suggest that the complement system utilizes C3 to guard not only extracel
288 century after the significance of the human complement system was recognized, we have come to realiz
289 tubular epithelial cells (TECs) control the complement system, we examined the expression of complem
290 ta-fibrils in Alzheimer disease activate the complement system, we have here investigated specific in
291 including acute-phase response signaling and complement system) were overexpressed in the follicular
292 CRPs, which protect cells from attack by the complement system, were lower in abca4(-/-) versus wild-
295 indings provide initial evidence linking the complement system with cortical thinning in humans, a pr
296 During sepsis, excessive activation of the complement system with generation of the anaphylatoxin C
297 ial sepsis triggers robust activation of the complement system with subsequent generation of anaphyla
298 study, we demonstrated the importance of the complement system within the CNS in the development of b
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
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