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1 iable immunodeficiency syndrome (a defect in antibody formation).
2 t appear to predispose to resistance through antibody formation.
3 late ongoing immune responses independent of antibody formation.
4 e germinal centre reaction and high affinity antibody formation.
5 hile preventing rejection and donor-specific antibody formation.
6  diversity as does genetic recombination and antibody formation.
7 o study cellular and molecular mechanisms of antibody formation.
8  allograft tissues to promote donor-specific antibody formation.
9  region of the PLA2R1 gene may contribute to antibody formation.
10 ody after AMR therapy and the absence of new antibody formation.
11           No patient developed antigaliximab antibody formation.
12 cant association with de novo posttransplant antibody formation.
13 here was no evidence of host antitrastuzumab antibody formation.
14 related expression of hFIX without anti-hFIX antibody formation.
15 resulted in 500 ng/mL hFIX in plasma without antibody formation.
16 ogy), and participant incidence of denosumab antibody formation.
17  monitored for tumor response, toxicity, and antibody formation.
18 on therapy completely inhibited anti-hamster antibody formation.
19 ormalizes peripheral platelet counts without antibody formation.
20 pCMV-LacZ did not inhibit IgE anti-ovalbumin antibody formation.
21 y Response Evaluation Criteria, and antidrug antibody formation.
22 s important to devise strategies to modulate antibody formation.
23 ression declines over time in the absence of antibody formation.
24           We found a high incidence of PRT/H antibody formation (29%) in patients undergoing cardiac
25    Immune tolerance was confirmed by lack of antibody formation after repeated challenges with cFVIII
26     Plasma concentrations of both agents and antibody formation against both agents were also assesse
27  a period of 17-18 days enable assessment of antibody formation against the human Tf component of the
28  engineer antigen-specific Tregs to suppress antibody formation against the soluble therapeutic prote
29 emonstrate that EPO inhibits T(FH)-dependent antibody formation, an observation with potential implic
30 as a predictor of de novo donor-specific HLA antibody formation and antibody-mediated rejection.
31 matched human leukocyte antigens, as well as antibody formation and antibody-mediated rejection.
32  and transfusion reactions, volume overload, antibody formation and coagulation derangements.
33 f PEGasp is an effective approach to prevent antibody formation and inactivating hypersensitivity rea
34         Adverse reactions to therapy include antibody formation and infusion reactions, infections, a
35 e determined the prevalence of self-reactive antibody formation and its regulation in human B cells.
36                       At 3 months, anti-drug antibody formation and low adalimumab concentrations wer
37 s persistence correlated with poor anti-hAAT antibody formation and minimal hepatocyte toxicity.
38                                           No antibody formation and T-cell responses to FIX-R338L wer
39 B cell and macrophage reactions culminate in antibody formation and TGF-beta secretion, respectively,
40 y-stimulating factor-cytokines involved with antibody formation and type 2 immune responses.
41 thin donor grafts, diminished donor-specific antibody formation, and delayed rejection of subsequent
42 uman immunodeficiency virus (HIV) may impair antibody formation, and false-negative hepatitis C virus
43 g-term expression of FVIII, without apparent antibody formation, and improved the phenotype of hemoph
44 ng salivary bacterial burdens, corresponding antibody formation, and periodontitis severity than A. a
45 bution, blood circulation time, neutralizing antibody formation, and targeted delivery ability of the
46              We determined allergen-specific antibody formation by analysis of the germinal center re
47  to the acute immune activation and anti-PEG antibody formation commonly observed with lipid nanopart
48  uncovered 5 suggestive loci for antinuclear antibody formation, consisting of 3 dominant NZB contrib
49 feron, and the incidences of anti-interferon antibody formation did not significantly differ among th
50 f-reactive T cell enhanced activity and auto-antibody formation enabled by PD-1/PD-L1 blockade, leadi
51 cient mice demonstrated enhanced T-dependent antibody formation especially of IgE isotype and allergi
52  (7%) ( P = 0.12) and de novo donor-specific antibody formation (H+M+ 24%; H+M- 10%; P = 0.13).
53 ic systemic immune suppression of pathogenic antibody formation (immunoglobulin [Ig] 1/inhibitors, Ig
54 ese findings plus the lack of donor-specific antibody formation imply that prolonged graft survival w
55 ll costimulatory signals for antifactor VIII antibody formation in a murine model of hemophilia A.
56 ant forms of Hb have been shown to stimulate antibody formation in a variety of animal species.
57  when aberrantly regulated, drive pathogenic antibody formation in autoimmunity and undergo neoplasti
58 sis revealed a low incidence of neutralizing antibody formation in both groups.
59  address serious complications of inhibitory antibody formation in current replacement therapy, we cr
60 ntial utility to treat anti-FVIII inhibitory antibody formation in hemophilia A patients.
61 entified novel genetic markers of inhibitory antibody formation in hemophilia patients that may ultim
62    These data demonstrate increased anti-CCP antibody formation in HLA-DR4-positive patients with pol
63 AA activity in plasma and prevented anti-GAA antibody formation in immunocompetent GAA-knockout mice
64                   HA22-LR-8M does not induce antibody formation in mice when given repeatedly by intr
65 al element of the clonal selection theory of antibody formation in order to explain tolerance of self
66 individuals correlates with the frequency of antibody formation in patients with normal immune system
67 The stabilized oligomers were used to induce antibody formation in rabbits.
68             There was a marked difference in antibody formation in the two strains of mice; 100% of t
69 database was assessed for cases of antidonor antibody formation in tolerant animals over the last 20
70 ith respect to its poor biodegradability and antibody formation, including new evidence about preform
71                                   Inhibitory antibody formation is a major complication of factor VII
72 e free ("active") drug concentration and the antibody formation is critical for preclinical and clini
73                 However, circumstances where antibody formation is impaired after vaccination, such a
74 y all patients with HIT/T, it is unclear how antibody formation is initiated, why only a small subset
75 llowing HOD RBC transfusion, suggesting that antibody formation is not dependent on the splenic folli
76                       These include impaired antibody formation; loss of delayed cutaneous hypersensi
77 ppressing cell-mediated immune responses and antibody formation, major factors in acute and chronic r
78                               Although rare, antibody formation may occur in the treatment of other c
79                                     Delay of antibody formation may prolong infectivity.
80 sinic:polycytidylic acid enhanced anti-FVIII antibody formation, MZ B-cell depletion continued to dis
81 d showed similar patterns of anti-adenovirus antibody formation, only Balb/c and C3H mice developed s
82 pressed therapeutic levels of FVIII, without antibody formation or other toxicities, for more than 3
83 e patients had no increased frequency of new antibody formation posttransplant.
84  in addition to steroids to prevent anti-AAV antibody formation.RESULTSGroup 1 participants had a rap
85 , results in significantly higher anti-FVIII antibody formation, suggesting that the increased levels
86  recovery but that neutralizing anti-PIXY321 antibody formation suppressed the hematologic and bioche
87 h revealed domain contributions to secretory antibody formation, these results provide detailed model
88 priming of mice with pCMV-LacZ prevented IgE antibody formation to a subsequent i.p. beta-gal in alum
89 ministration of vectors may avoid inhibitory antibody formation to factor VIII (FVIII) by taking adva
90 ctivity reaching 25% to 40% activity without antibody formation to FIX.
91 tion of CD4(+)CD25(+)GITR(+) that suppresses antibody formation to FIX.
92 her genetic factors may increase the risk of antibody formation to functional F.IX.
93 as been stable for >1 year (ongoing) without antibody formation to the cFVII transgene.
94  depletion of CD4(+)CD25(+) T(regs) leads to antibody formation to the FIX transgene product after he
95 nsfusion on the breadth and magnitude of HLA antibody formation using current, sensitive, HLA-specifi
96 econdary, T cell-dependent and T-independent antibody formation using in vitro culture systems, murin
97 s that differ in size and/or zeta potential, antibody formation varies inversely with heparin concent
98                                 Anti-PIXY321 antibody formation was assessed by enzyme-linked immunos
99      The effect of neonatal gene transfer on antibody formation was determined using a retroviral vec
100                     After protein challenge, antibody formation was markedly reduced for animals that
101  patients (P = .004), de novo donor-specific antibody formation was seen in 40% (17/42) vs 2.7% (P <
102 mmune responsiveness to CEA, as reflected by antibody formation, was not detectable in transgenic mic
103 ng burden of disease arising from the HLA-DQ antibody formation, we suggest that HLA-DQalphabeta shou
104 immune cell infiltration, and donor-specific antibody formation were analyzed.
105 ited immunoglobulin M (IgM) and IgG anti-HOD antibody formation, whereas CD4 T-cell depletion only pr
106 pression of canine G-CSF caused neutralizing antibody formation which precluded long-term increases i
107 t gold-standard diagnostic tests relies upon antibody formation, which is typically delayed and thus

 
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