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1 table surrogate marker for the prediction of complement binding.
2 intrinsically disordered, and is involved in complement binding.
3  by tumor necrosis factor alpha and inhibits complement binding.
4 hanced survival in human serum and decreased complement binding.
5 lex formation, a PXXP motif in HPK1 strongly complements binding.
6  against SHIV challenge when Fc receptor and complement-binding activities are engineered out of the
7 rescence-to-cutoff ratios >5 correlated with complement binding activity, whereas values <5 denoted c
8 tivity is associated with the elimination of complement binding alone.
9 e protection of the nanocarrier surface from complement binding and activation.
10                     Compared with the strong complement binding and CDC with Abs against glycolipids
11 35A, P329G (LALA-PG) variant that eliminates complement binding and fixation as well as Fc-gamma-depe
12 wcaJ led to increased complement resistance, complement binding, and opsonophagocytosis, which may pr
13           However, the clinical relevance of complement-binding anti-HLA antibodies remains unclear.
14 -, and IgG-Luminex, to assess or predict the complement-binding capability of HLA IgG antibodies.
15 High levels of anti-HLA antibodies and their complement binding capacity were associated with increas
16                  We investigated whether the complement-binding capacity of anti-HLA antibodies plays
17                            Assessment of the complement-binding capacity of donor-specific anti-HLA a
18 donor-specific anti-HLA antibodies and their complement-binding capacity.
19 m of this study was to determine the further complement-binding characteristics of the most harmful D
20                            The extracellular complement-binding (CUB) and coagulation factor domains
21 main binds to the amino-terminal quarter, or complement-binding (CUB) domain, of Npn-1.
22                                              Complement binding decreased from the double-positive th
23                                              Complement binding decreased with development and matura
24                       Therefore, we assessed complement binding, deposition, and complement-dependent
25 m protease inhibitor that contains potential complement-binding domains, and has been shown to improv
26 al (54%), as compared with patients with non-complement-binding donor-specific anti-HLA antibodies (9
27                              The presence of complement-binding donor-specific anti-HLA antibodies af
28                                Patients with complement-binding donor-specific anti-HLA antibodies af
29                                       Adding complement-binding donor-specific anti-HLA antibodies to
30          The presence of de novo persistent, complement-binding DQ DSA negatively impacts kidney allo
31 tation detection, monitoring, and removal of complement-binding DQ might be crucial for improving lon
32                                              Complement-binding DSA per se were not significantly ass
33            Solid-phase assays to distinguish complement binding from noncomplement binding HLA-specif
34 tage, and within single-positive thymocytes, complement binding gradually decreased with increasing i
35 ck of antiinflammatory IgA, and an excess of complement-binding IgG and IgM Abs, will promote inflamm
36 sult does not indicate the absence of strong complement-binding IgG subclasses.
37 an fluorescence intensity [MFI]>500), strong complement-binding IgG1 and IgG3 subclasses accounted fo
38 ves prediction of C1q binding likely because complement-binding IgG1 and IgG3 subclasses dominate reg
39 man leukocyte antigen antibodies with strong complement-binding IgG1 and IgG3 subclasses.
40                                      Neither complement binding in vitro nor antigen-antibody binding
41 nst microbes, such as opsonophagocytosis and complement binding, negatively correlated with antibody
42                  One of these, extracellular complement binding protein (Ecb), is known to interfere
43                The virus encodes homologs to complement-binding proteins, three cytokines (two macrop
44 n was dose dependent and was reproduced in a complement binding reaction consisting of six purified p
45 ns, Fw contains a lectin-binding domain, ten complement binding repeats, and a transmembrane domain.
46 utralizing but not Fc receptor-activating or complement-binding responses.
47 ket on the SH3C while several other residues complement binding through hydrophobic interactions, cre
48 treatment is likely due to the prevention of complement binding to aggregates or dissociation of aggr
49 rum samples from patients treated with IVIg, complement binding to and lysis of complement-sensitive
50    Altogether, these molecular insights into complement binding to surface-bound IgGs could be import
51 nd CDC with Abs against glycolipids and KSA, complement binding was diminished with Abs against mucin
52          During this period of time, IgM and complement binding were observed within the graft, as we