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1 lement factor 1q (C1q) and activation of the classical complement pathway.
2 ts C1r and C1s of the first component of the classical complement pathway.
3 n through C1q fixation and activation of the classical complement pathway.
4 ace that recruit natural IgM to initiate the classical complement pathway.
5 so can bind C1q and act as inhibitors of the classical complement pathway.
6 lity of FX to protect Ad5 from attack by the classical complement pathway.
7 lization was mediated by natural IgM and the classical complement pathway.
8 ollate injection, suggesting a defect in the classical complement pathway.
9 s to apoptotic cells, thereby activating the classical complement pathway.
10 ling of the lptA mutant occurred through the classical complement pathway.
11 s, which triggered activation of C1q and the classical complement pathway.
12 f C5 but not of downstream components of the classical complement pathway.
13 h FcgammaRI and FcgammaRII and activates the classical complement pathway.
14 rarely with IgM indicating activation of the classical complement pathway.
15 great extent on its ability to activate the classical complement pathway.
16 mplement components C1q, C1r, and C1s of the classical complement pathway.
17 dothelium of the graft and activation of the classical complement pathway.
18 to GBS was associated with activation of the classical complement pathway.
19 h immune complex dependent activation of the classical complement pathway.
20 that sialylation may indirectly regulate the classical complement pathway.
21 min) mediated through the antibody-dependent classical complement pathway.
22 in diseases accompanied by the activation of classical complement pathway.
23 ins, indicating a role for components of the classical complement pathway.
24 iphery by the activation and fixation of the classical complement pathway.
27 gG3-triggered CML and to force a switch from classical complement pathway activation to C1q-dependent
29 totoxic IgM anti-mouse antibodies and strong classical complement pathway activity with minimal alter
30 teps of complement and effectively depressed classical complement pathway activity, alternative compl
31 C1q is the target recognition protein of the classical complement pathway and a major connecting link
32 imannan immunoglobulin G (IgG) activates the classical complement pathway and accelerates initiation
33 s open a connection between the inflammatory classical complement pathway and connective tissue homeo
34 plement C1q protein, thereby attenuating the classical complement pathway and facilitating pneumococc
36 was protective in mice lacking a functional classical complement pathway and show that alternative c
38 and C1s, proteases required to activate the classical complement pathway, and C3 showed a significan
39 h C1q, leading to a strong activation of the classical complement pathway, and results in consumption
40 for exploring CRP-mediated activation of the classical complement pathway, and that the characteristi
41 s rapid and is mediated by components of the classical complement pathway; and that gC mainly protect
42 addition to AMR-triggered activation of the classical complement pathway, antibody-dependent cellula
43 vation but have fully active alternative and classical complement pathways, are protected from cardia
44 nonoverlapping epitopes, which activates the classical complement pathway as well as inhibits fH bind
47 that elicits serum antibodies that activate classical complement pathway bacteriolysis and also inhi
48 expressed in eukaryotic cells activated the classical complement pathway but not the alternative or
52 The results indicated that activation of the classical complement pathway (CCP) was a primary mechani
53 in and C1q, the recognition component of the classical complement pathway (CCP), which results in the
54 ndicated that genetic variation within early classical complement pathway components (C1q, C1r, and C
56 cantly more resistant to antibody-dependent, classical complement pathway-directed bacteriolysis than
57 etic deficiencies of early components of the classical complement pathway (e.g., C1q, C4, and C2) are
58 ulted in normal functional properties of the classical complement pathway followed by reduced severit
59 at the characteristic of CRP to activate the classical complement pathway has no role in protecting m
60 ave been previously reported to activate the classical complement pathway in an antibody-independent
63 de the first direct genetic evidence for the classical complement pathway in the induction of EAMG in
64 cteria can activate both the alternative and classical complement pathways in the absence of specific
65 CMV-infected fibroblasts activated via the classical complement pathway independent of specific ant
66 time of human platelet-poor plasma or in the classical complement pathway, indicating that it is a sp
69 tly, mice that lack a major component of the classical complement pathway initiation complex (C1q) bu
75 s to the donor endothelium that activate the classical complement pathway, it was hypothesized that p
76 bular head region of C1q and to initiate the classical complement pathway, leading to activation of C
77 q-dependent C4b deposition on live bacteria (classical complement pathway), only those antibodies tha
78 opulation of the alternative rather than the classical complement pathway, previously not appreciated
80 ), a meningococcal vaccine antigen, activate classical complement pathway serum bactericidal activity
81 ed to inhibit IgM-mediated activation of the classical complement pathway, since survival of the tspB
82 nd altered self components, and triggers the classical complement pathway through activation of its a
83 um against N. gonorrhoeae is mediated by the classical complement pathway through an antibody-depende
84 cognize microbial pathogens and activate the classical complement pathway through C1q (refs 3 and 4).
85 lternative complement pathway as well as the classical complement pathway; trigger the formation of c
86 ermatomyositis result from activation of the classical complement pathway triggered by direct binding
89 ese data indicate that ethanol activates the classical complement pathway via C1q binding to apoptoti
90 r, these data suggest that initiation of the classical complement pathway via C1q is detrimental to r
91 le levels, suggesting that activation of the classical complement pathway was not required for innate
93 binding site of SpA and 2) proceeded via the classical complement pathway, we tested a panel of monoc
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