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1 e cases had monotypic deposits (i.e., type I cryoglobulin).
2 56% had type II, 29% type I, and 8% type III cryoglobulin.
3 actosylation and sialylation, in relation to cryoglobulin activity, to the nephritogenic potential of
4 genic potential of 6-19 IgG3 by limiting its cryoglobulin activity.
5 leads to formation of large amounts of mixed cryoglobulins and a systemic inflammatory injury that re
6  HCV is specifically concentrated in type II cryoglobulins and has been implicated in the cutaneous v
7                                    HCV load, cryoglobulins, and cytokines were quantified by flow cyt
8  sera, HCV, but not HGV, was concentrated in cryoglobulins, and HCV, but not HGV, correlated with cry
9 in rashes, renal abnormalities, and elevated cryoglobulins, and was receiving interferon-alpha at the
10                                              Cryoglobulins are cold-precipitating immunoglobulins tha
11                                        Mixed cryoglobulins are complexes of immunoglobulins that reve
12                            Circulating mixed cryoglobulins are detected in 40%-60% of patients with h
13           HCV-MCS was defined by circulating cryoglobulin associated with systemic vasculitis symptom
14              Here, we used the 6-19 model of cryoglobulin-associated GN to define the relative contri
15  the role of FcgammaRIIb in a mouse model of cryoglobulin-associated membranoproliferative glomerulon
16 eginning at weaning suppressed production of cryoglobulin, attenuating both the renal injury and syst
17                                Because serum cryoglobulins (CG) are known to be associated with an in
18                        In only one case were cryoglobulins detected (at low titer and on only one of
19                                              Cryoglobulins differ in their composition, which has an
20                                        These cryoglobulins form crystals, and we measured their solub
21 ion and the underlying disease that triggers cryoglobulin formation.
22 ts for more than 97% of the mouse Ig in this cryoglobulin; furthermore, glomerular disease develops w
23 lpha-fetoprotein >10 ng/ml in 2/8 (25%), and cryoglobulins >50 microg/ml in 3/6 (50%) infected with H
24 liferative glomerulonephritis); hematologic (cryoglobulin, Hodgkin's and non-Hodgkin's lymphoma [NHL]
25 ex deposits and higher levels of circulating cryoglobulins, IgG2a, IgG2b, and IgM, compared with TSLP
26 s such as anti-double stranded DNA titers or cryoglobulin IgG3 levels, circulating immune complex lev
27 munofluorescence with regards to the type of cryoglobulin in 47% of cases.
28 vasculitis [CV]) caused by the deposition of cryoglobulins in blood vessels.
29   HCV is selectively precipitated by type II cryoglobulins in coinfected sera.
30                               No patient had cryoglobulins in the blood or kidney.
31 inct entity characterized by the presence of cryoglobulins in the serum.
32    Our results suggest that in this model of cryoglobulin-induced glomerulonephritis the neutrophil i
33 d the role of complement in a mouse model of cryoglobulin-induced immune complex glomerulonephritis.
34                               Patients' mean cryoglobulin level decreased from 0.56 +/- 0.18 at basel
35                                              Cryoglobulin levels correlated with in vivo proliferatio
36                                              Cryoglobulin levels decreased in 89% of patients, with m
37                               In conclusion, cryoglobulins may be a useful prognostic indicator for i
38 y disappearing in four of nine cases who had cryoglobulins measured after treatment.
39 f IgG sialylation against the development of cryoglobulin-mediated GN, highlighting the anti-inflamma
40 pitate in C57BL/6 mice consisted of the IgG3 cryoglobulin only (type I cryoglobulinemia) compared wit
41 rus (HCV) infection develop detectable serum cryoglobulins or cryoprecipitates (CP), although most do
42                       Seven patients cleared cryoglobulins out of 15 who were initially positive.
43          We report a study of monoclonal IgG cryoglobulins overexpressed by two patients with multipl
44 s of Tfh cells (P = .03) and serum levels of cryoglobulin (P = .01).
45 tor activity, C4 fraction of complement, and cryoglobulin; peripheral blood mononuclear cells were is
46                       These changes promoted cryoglobulin production and immune complex-mediated rena
47 c mice with established MPGN also diminished cryoglobulin production and reversed the renal and syste
48 decreased renal scores as well as lower IgG3 cryoglobulin production and vasculitis.
49 e bone marrow likely caused the reduction in cryoglobulin production.
50 ll-defined and cases with undetectable serum cryoglobulin (seronegative CryoGN) have not been investi
51                                              Cryoglobulins showed HCV, monomeric IgM, and monomeric I
52 line to 0.21 +/- 0.14 g/L at week 36, and no cryoglobulin was detected in 50% of patients at this tim
53                   Serum HCV was quantitated, cryoglobulins were analyzed by column chromatography at
54                                      Type II cryoglobulins were detected in the sera of all 3 patient
55 on of 6-19 hybridoma cells producing an IgG3 cryoglobulin with rheumatoid factor activity against IgG
56  in mice results in the development of mixed cryoglobulins, with renal involvement closely resembling