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1 ucidate the interaction and stability of the antigen-antibody complex.
2 a rare view of antigen flexibility within an antigen:antibody complex.
3 nt is protected from inflammation induced by antigen-antibody complexes.
4 ic antibodies via differential catabolism of antigen-antibody complexes.
5 nity through activation of effector cells by antigen-antibody complexes.
6 sslinking produced the increased affinity of antigen-antibody complexes.
7 thermodynamically characterize high-affinity antigen/antibody complexes.
8 tion of individual antigens, antibodies, and antigen/antibody complexes.
9 bodies are capable of using metals to bridge antigen:antibody complexes.
10 Second, to define the k(d) of this stable antigen/antibody complex accurately, the highest PSA con
11 e, we analyzed an internalization process of antigen-antibody complexes after binding of RSV-specific
12 al pathway of complement activated by, e.g., antigen-antibody complexes, also recognizes the C4 C345C
14 ith HyHEL-63 in the crystal structure of the antigen-antibody complex, and 10 HyHEL-63 residues in co
16 these results show that neither B cells nor antigen-antibody complexes are essential for the mainten
17 e to a variety of situations in which stable antigen-antibody complexes are formed in the presence of
18 of pathway blockade, the organization of the antigen-antibody complexes at the cell surface, and oppo
19 report is the first to provide evidence that antigen-antibody complexes bind specifically to apoptoti
21 tor on T cells as soluble shed antigen or as antigen-antibody complexes, causing impairment in the ac
22 (1) and one in this issue, demonstrate that antigen-antibody complexes containing RNAs activate B ly
25 mice may translate to a lack of toxicity of antigen-antibody complexes during the course of infectio
27 B) by the Ig crystallizable fragment (Fc) in antigen-antibody complexes held on FDCs decreases the ac
30 mmunofluorescence analyses revealed granular antigen-antibody complexes in a subepithelial location a
31 Previous studies demonstrated that specific antigen-antibody complexes in the sera of patients with
33 n presentation by B cells and persistence of antigen-antibody complexes on follicular dendritic cells
34 antigen and the capacity to form multivalent antigen-antibody complexes on target cells were key dete
35 cence (ECL) with exposure to X-ray film, the antigen-antibody complexes on the blot are reacted with
38 ms associated with limited proteolysis of an antigen-antibody complex particularly in the vicinity of
39 formed on each platform with three different antigen/antibody complexes possessing nanomolar to picom
42 depends on extensive structural analyses of antigen-antibody complexes.Single-particle electron cryo
45 n A linked to Sepharose were used to isolate antigen-antibody complexes that contained few contaminat
46 system to couple receptors for antigens and antigen-antibody complexes to adaptive and innate immune
48 ctroscopy (EIS) in which the formation of an antigen-antibody complex was quantified as a function of
49 three of these subpopulations of pAbs formed antigen-antibody complexes which could be isolated by ge
50 refolded antibodies were capable of forming antigen-antibody complexes which could be isolated by ge
53 nd genetic studies coupling the structure of antigen-antibody complexes with their antiviral function
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