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1 the presence of blocking Abs to FcgammaR and complement receptor.
2 fects B lymphocytes through their CD21 (CR2) complement receptor.
3 be eliminated by microglial cells expressing complement receptors.
4 sulting in vesicle recognition by macrophage complement receptors.
5 Ig receptors (FcRgammaI and FcgammaRIII) or complement receptors.
6 sonization and binding of these complexes to complement receptors.
7 , FcgammaRIV, the inhibitory FcgammaRIIB and complement receptors.
8 psonized particles become immune adherent to complement receptor 1 (CR1 or CD35) on human erythrocyte
9 ly lack the third component of complement or complement receptor 1 (CR1) and CR2 developed increased
10 levels of E-bound Abs, reduced E-associated complement receptor 1 (CR1) and decay-accelerating facto
16 ng protein-like homologue 4 (PfRh4) binds to complement receptor 1 (CR1) to mediate entry of malaria
18 omplement-regulatory proteins, in particular complement receptor 1 (CR1), are important in the pathog
19 geted Cr2(-/-) mice, which lack both CR2 and complement receptor 1 (CR1), have demonstrated contradic
24 D55), membrane cofactor protein (MCP, CD46), complement receptor 1 (CR1, CD35) and viral molecules su
25 r primates are unique among mammals in using complement receptor 1 (CR1, CD35) on red blood cells (RB
27 ce or absence of blocking Abs to CD23, CD32, complement receptor 1 (CR1, CD35), and/or CR2 (CD21) was
31 ned approach was augmented by adding soluble complement receptor 1 (sCR1) to the perfusate in one fur
32 D47-blocking antibody (alphaCD47Ab), soluble complement receptor 1 (sCR1), and recombinant thrombomod
33 tabilized C3bBb and perturbed C3b binding to complement receptor 1 but did not perturb binding to fac
34 the recognition of deposited C3 fragments by complement receptor 1 even when the absolute number of C
35 -tetanus toxoid antibody levels, erythrocyte complement receptor 1 expression, and lymphocyte prolife
36 ynonymous SNP, rs6691117 (Val-->IIe), in the complement receptor 1 gene (CR1) was associated with ESR
37 s functions analogously to human erythrocyte complement receptor 1 in its role to traffic immune comp
38 up had a progressive increase in erythrocyte complement receptor 1 levels compared with baseline (P =
40 o evaluate new therapeutic targets employing complement receptor 1 peptide homologues and the antimac
41 the functional analogue to human erythrocyte complement receptor 1 with a role that is distinct from
43 lowed us to discover that expression of CR1 (complement receptor 1), an AD susceptibility gene involv
44 factors, such as decay accelerating factor, complement receptor 1, and factor H, which directly inte
45 tors, such as factor H, C4b-binding protein, complement receptor 1, and membrane cofactor protein.
46 on host cells by the complement system, and complement receptor 1-like protein y (CRRY) is an import
49 In a model system in which RBCs deficient in complement receptor 1-related gene/protein y (Crry) are
50 of either decay-accelerating factor (DAF) or complement receptor 1-related gene/protein y (Crry) on m
51 lement inhibition with complement receptor 2-complement receptor 1-related protein y (CR2-Crry, an in
52 This phenotype, which shared features with complement receptor 1-related protein Y (Crry) depletion
54 ow that deleting the C3 convertase regulator complement receptor 1-related protein y (Crry) induces m
56 lement-regulatory protein (CRP) (CD55, CD46, complement receptor 1-related protein y/CD46) expression
63 complexes (ICs) from noncognate B cells via complement receptors 1 and 2 (CD35 and CD21, respectivel
66 lly depleted of complement, or deficient for complement receptors 1 and 2, were also susceptible to s
67 that FPR activation leads to upregulation of complement receptors 1 and 3 as well as FCgamma receptor
68 on with (99m)Technecium-labelled recombinant complement receptor 2 ((99m)Tc-rCR2), which specifically
69 ntibody assay, we found that viral gp350 and complement receptor 2 (CD21) are required for CD3(+) T-c
72 of complement component C3d with B or T cell complement receptor 2 (CR2 or CD21) is a link between in
73 inant mouse protein composed of domains from complement receptor 2 (CR2) and FH (CR2-FH) in two model
74 consisting of the iC3b/C3d-binding region of complement receptor 2 (CR2) and the inhibitory domain of
75 mia-reperfusion (IR)-induced damage requires complement receptor 2 (CR2) for generation of the approp
76 receptor(s), we found that App1 does bind to complement receptor 2 (CR2) in a dose-dependent manner.
77 eraction between complement fragment C3d and complement receptor 2 (CR2) is a key aspect of complemen
78 ntains the AP-inhibitory domain, linked to a complement receptor 2 (CR2) targeting fragment that bind
79 nking an iC3b/C3dg-binding fragment of mouse complement receptor 2 (CR2) to a mouse complement-inhibi
80 cantly enhanced when linked to a fragment of complement receptor 2 (CR2), a receptor that targets C3
83 le of inhibiting the interaction of C3d with complement receptor 2 (CR2), which plays an important ro
85 , targeted complement inhibition with either complement receptor 2 (CR2)-Crry (blocks all pathways at
90 nt that can facilitate the coligation of the complement receptor 2 (CR2/CD21) with the BCR via C3dg/A
94 ect of a recombinant AP inhibitor containing complement receptor 2 and factor H (CR2-fH) on CAIA in m
95 ed in the lung and occurred independently of complement receptor 2 and Fcgamma receptors, but was dep
96 that contains the iC3b/C3d binding region of complement receptor 2 linked to the inhibitory region of
99 potential HIV-binding molecules FcRgammaIII, complement receptor 2, and various complement components
100 3) deficiency and complement inhibition with complement receptor 2-complement receptor 1-related prot
103 21/35(-/-) mice, deficient in CD21 and CD35 (complement receptors 2 and 1, respectively), were infect
104 omplement component C3 (C3d) and the modular complement receptor-2 (CR2) is important for cross-linki
105 rHDL attenuated the amount of CC-induced complement receptor 3 (CD11b/CD18) expression on monocyt
107 e is dependent on beta-glucan recognition by complement receptor 3 (CD11b/CD18), but not Dectin-1, or
108 ement activation resulted in upregulation of complement receptor 3 (CD11b/CD18), leading to phagocyto
109 dition to the I-domain, the beta(2) integrin complement receptor 3 (CR3) (CD11b/CD18) contains a lect
110 gested that beta2 integrin receptors such as complement receptor 3 (CR3) and 4 (CR4) may act as novel
116 ized C albicans was found to be dependent on complement receptor 3 (CR3) and the signaling proteins p
118 s also unaffected in mice deficient in C3 or complement receptor 3 (CR3) but was almost completely ab
123 we uncovered a novel role for the microglial complement receptor 3 (CR3) in the regulation of soluble
124 with the complement C3dg, can interact with complement receptor 3 (CR3) on activated monocytes, thus
125 ion resulted in reduced bacterial binding to complement receptor 3 (CR3) on the surface of murine mac
128 ecifically iC3b production and engagement of complement receptor 3 (CR3), had a significant impact on
129 ophages isolated from mannose receptor (MR), complement receptor 3 (CR3), MyD88, Toll-like receptor 4
130 ional and oligomeric states: the BCR and the complement receptor 3 (CR3), on murine splenocytes, puri
131 identified complement receptor CRIg, but not complement receptor 3 (CR3), rescued DAF/Crry-deficient
133 ially binds an inactive form of the integrin complement receptor 3 (CR3), using a site outside of its
137 orming RTX cytolysin (Hly) moiety, binds the complement receptor 3 (CR3, alpha(M)beta(2), CD11b/CD18,
138 rior studies indicated the ability of Abs to complement receptor 3 (CR3, CD11b/CD18) to suppress the
139 D209), Dectin-1, Toll-like receptors (TLRs), complement receptor 3 (CR3, CD11b/CD18), nucleotide olig
140 C. albicans mediated by the beta2 integrin, complement receptor 3 (CR3, CD11b/CD18, alphaMbeta2).
143 the fimbriae of P. gingivalis interact with complement receptor 3 (CR3; CD11b/CD18) in monocytes/mac
144 been shown to function via the iC3b-receptor complement receptor 3 (CR3; CD11b/CD18) thereby enhancin
146 neutrophil opsonic receptors, FcgammaRs and complement receptor 3 (Mac-1) to cellular cytotoxic resp
148 roglial phagocytosis stimulated by fAbeta or complement receptor 3 and argue that this may, in part,
149 modulation of TLR8 signaling was mediated by complement receptor 3 and led to enhanced infection.
150 roduce a new picture of Fcgamma receptor and complement receptor 3 intracellular signaling have been
151 ae allowed P. gingivalis to exploit the TLR2/complement receptor 3 pathway for intracellular entry, i
154 ITGAM encodes the integrin CD11b, a part of complement receptor 3, a novel candidate gene implicated
156 egrin (CD11b/CD18), macrophage-1 antigen, or complement receptor 3, as a cellular receptor for leukoc
157 lex with its receptor (the alpha-I domain of complement receptor 3, CD11b-I), both for the human and
158 ound to depend on beta-glucan recognition by complement receptor 3, require Fn and ERK but not ROS, a
159 MN with C5a led to upregulation of activated complement receptor 3, resulting in enhanced complement
160 complement receptor 3, resulting in enhanced complement receptor 3-dependent PMN-ADCC against tumor c
161 mma receptor internalization pathway but not complement receptor 3-dependent uptake, which is control
164 Furthermore, overexpressing stathmin reduces complement receptor 3-mediated phagocytosis and cellular
167 1 in macrophages that lack mannose receptor, complement receptors 3 and 4, type A scavenger receptor,
168 g, attributed to diminished AM expression of complement receptor-3 (CR3), which is exploited by P. gi
171 colonization is associated with a variant of complement receptor 5a, the cellular target of the lukS
176 possible effects of ANE on the expression of complement receptors and Fc receptors were examined usin
177 activation did not promote infection through complement receptors and inhibited anti-H IgG-mediated e
178 is by macrophages is strongly dependent upon complement receptors and upon serum with intact compleme
179 entiates among the contributions from Fc and complement receptors, and provides a tool for estimating
181 in 8 (aqp8), adrenomedullin receptor (admr), complement receptor C1qR-like (crl), scavenger receptor
182 All measures were reversed by blocking C3a complement receptor (C3aR), alternative complement pathw
183 ional roles for both C5a receptors, that is, complement receptor C5a (C5aR) and C5a receptor-like 2 (
186 d an intimate crosstalk between TLR2 and the complement receptor C5aR and can contribute to the persi
188 deficient in complement factor 5 (C5) or the complement receptor C5aR mounted robust IL-17A responses
191 CXCR2 and CCR2 as targets for HlgAB, and the complement receptors C5aR and C5L2 as targets for HlgCB.
194 brane movement impedes the clustering of the complement receptor CD11b/CD18 on PMNs and, in turn, dec
196 radiation bone marrow-chimeric mice lacking complement receptors CD21 and CD35 on stromal cells elic
201 human T cells, autocrine stimulation of the complement receptor CD46, and specifically its intracell
204 lls (FDCs) and complement receptor (Cr)1 and complement receptor (Cr)2 are important for the generati
209 terium kansasii enter macrophages, using the complement receptors CR1, CR3, CR4, and the mannose rece
211 n, but not murine, erythrocytes also present complement receptor (CR1), which binds Ad5 in the presen
212 NE significantly inhibited the production of complement receptors (CR1, CR3, and CR4) and Fc receptor
215 ulating humoral immunity largely through the complement receptor CR2, which forms a coreceptor on B c
216 hagocytosis, altered the distribution of the complement receptor CR3 (CD11b/CD18), enhanced the intra
218 Inhibition of C1q, C3, or the microglial complement receptor CR3 reduces the number of phagocytic
219 cteria from the mannose receptor (MR) to the complement receptor CR3, the scavenger receptor A (SRA),
222 ing or gene ablation of the newly identified complement receptor CRIg, but not complement receptor 3
224 the individual roles of the alphavbeta5 and complement receptors (CRs) in the phagocytosis and induc
228 ly, deficiency of CRIg, CR3, and other known complement receptors failed to prevent Crry-deficient er
229 y result from reduction of the expression of complement receptors, Fc receptors, and F-actin formatio
237 reactive antibodies, we examined the role of complement receptors in the production of alphaGal-speci
239 ocytic index was caused by interference with complement receptor ingestion as a consequence of satura
240 t role in clearing particles in circulation, complement receptors involved in this process have yet t
243 ved MPhi, we now identify CD11b as the major complement receptor mediating MPhi adherence to the larv
245 e was recently independently identified as a complement receptor of the Ig superfamily (CRIg) and was
246 a targeted complement inhibitor, comprising complement receptor of the Ig superfamily (CRIg) fused w
248 rophages characterized by high expression of complement receptor of the Ig superfamily (CRIg), a rece
249 SPECT/muCT) imaging using Nanobodies against complement receptor of the Ig superfamily (CRIg), found
250 lated with disease protection, including the complement receptor of the immunoglobulin superfamily (C
252 the identification and characterization of a Complement Receptor of the Immunoglobulin superfamily, C
253 pture of bacteria-platelet-complexes via the complement receptor of the immunoglobulin superfamily, C
254 tulated that surface-bound C3 interacts with complement receptors on alloreactive T cells or on antig
257 otein, resulting in enhanced phagocytosis by complement receptors on human alveolar macrophages.
259 lement complex and lowered the expression of complement receptors on monocytes in whole blood in resp
262 ansplant (day 2) together with inhibition of complement receptors prevents engraftment syndrome and a
263 tic index but increased phagocytosis through complement receptors rapidly compensated for this effect
265 eal injection of cobra venom factor (CVF) or complement receptor-related gene y (Crry)-Ig, a potent C
266 nhibition of C3 by overexpression of soluble complement receptor-related protein y in an AD mouse mod
269 igated whether App1 would also bind to other complement receptor(s), we found that App1 does bind to
270 zing complement regulator derived from human complement receptor type 1 (APT070) and then subjected t
271 (tPA) to a monoclonal antibody (mAb) against complement receptor type 1 (CR1) expressed primarily on
274 4) on the merozoite surface interacting with complement receptor type 1 (CR1, CD35) on the erythrocyt
276 ndertaken to determine whether soluble human complement receptor type 1 (TP10), a potent inhibitor of
277 resence of a cofactor such as factor H (fH), complement receptor type 1, membrane cofactor protein, o
280 complement regulator (SCR) domains, whereas complement receptor type 2 (CR2) has 15 SCR domains and
281 the Epstein-Barr virus glycoprotein gp350 by complement receptor type 2 (CR2) is critical for viral a
282 short complement regulator (SCR) domains of complement receptor type 2 (CR2) that bind to complement
283 protein containing the C3d-binding region of complement receptor type 2 (CR2) was then conjugated to
285 irst two short consensus repeats (SCR1-2) of complement receptor type 2 (CR2, CD21) and C3d in soluti
289 therapeutic fusion protein linking the human complement receptor type 2 (CR2/CD21) C3 fragment (C3fra
293 d and inactivated C3b, which are ligands for complement receptor type 2 (CR2/CD21), the aim of the cu
298 e the antibody response in mice deficient in complement receptor types 1 and 2 (CR1 and CR2) has rais
300 ant part of the innate immune system, namely complement receptors, with the central molecular mechani