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1 lting mutant rCB10T614P,A617E product became arthritogenic.
2 esulting mutant CB8P449T,E452A was no longer arthritogenic.
3 ot cause B. burgdorferi 25015 to become more arthritogenic.
4 esponses to stimulation with a citrullinated arthritogenic aggrecan peptide were detected in RA patie
5 long-term modulation of T cells specific for arthritogenic Ags.
6                 These findings indicate that arthritogenic alphavirus infection drives a unique myelo
7 isease signs in mice infected with a related arthritogenic alphavirus, Ross River virus, but not in m
8 culture-adapted strains of Sindbis virus, an arthritogenic alphavirus.
9  of new expression vectors for two Old World arthritogenic alphaviruses (Sindbis and Chikungunya viru
10                                              Arthritogenic alphaviruses are human pathogens maintaine
11 or functions that affect the pathogenesis of arthritogenic alphaviruses have not been defined.
12                                              Arthritogenic alphaviruses including Ross River virus (R
13 hritic infiltrates seen after infection with arthritogenic alphaviruses such as chikungunya virus.
14                                              Arthritogenic alphaviruses such as Ross River virus (RRV
15  a member of a globally distributed group of arthritogenic alphaviruses that cause weeks to months of
16 d Irf1 (-/-) mice with two distantly related arthritogenic alphaviruses, chikungunya virus (CHIKV) an
17 -1 in modulating pathogenesis of two related arthritogenic alphaviruses, chikungunya virus and Ross R
18                                              Arthritogenic alphaviruses, including Ross River virus (
19                                              Arthritogenic alphaviruses, including Ross River virus (
20                                   Like other arthritogenic alphaviruses, mechanisms of CHIKV pathogen
21                 Mice were inoculated with an arthritogenic amount of S. aureus intravenously or by lo
22 e antiviral activity of mouse Ifitm3 against arthritogenic and encephalitic alphaviruses using cells
23 1A(low) T cells were tissue-invasive and pro-arthritogenic, and MRE11A reconstitution mitigated synov
24 itiate disease by helping B cells to produce arthritogenic anti-glucose-6-phosphate isomerase (anti-G
25 is and is induced by well-defined monoclonal arthritogenic antibodies and enhanced by injection of li
26 ital imaging to demonstrate that transfer of arthritogenic antibodies caused macromolecular vasoperme
27 not rely on identification of the initiating arthritogenic antigen.
28 /c mice expressing a TCR that recognizes the arthritogenic ATEGRVRVNSAYQDK peptide of human cartilage
29 ease by providing help to B cells to produce arthritogenic autoantibodies.
30 d found to be supported by the cotransfer of arthritogenic autoantibodies.
31 ction as antigen-presenting cells (APCs) for arthritogenic autoantigens found within inflamed joint t
32 both the inhibition and amplification of the arthritogenic B cell response.
33                    The mechanisms applied to arthritogenic B cells expressing antigen-specific B cell
34       In patients with rheumatoid arthritis, arthritogenic B cells often up-regulate Bcl(XL) expressi
35 of the hybrids cross-reacted with either the arthritogenic CII 445-453 or murine CII.
36                               In these mice, arthritogenic cytokine may be produced by neutrophils th
37 une signals, including TLR4 agonists and the arthritogenic cytokine, IL-1beta, via an NFkappaB pathwa
38 can alter the spectrum of cells that produce arthritogenic cytokines.
39 verity of AA, despite responding well to the arthritogenic determinant within Bhsp65.
40 nal antibody therapy that aborted lethal and arthritogenic disease in wild-type and immunocompromised
41 vectored viruses that primarily cause either arthritogenic disease or acute encephalitis.
42 Alphaviruses are a reemerging viral cause of arthritogenic disease.
43 tion of HCG was initiated 2 days prior to an arthritogenic dose of streptococcal cell wall (SCW) in n
44 W (3 microg/day), initiated 7 days before an arthritogenic dose of systemic SCW, virtually eliminated
45 in normal adult articular cartilage, and the arthritogenic epitope(s) remains intact in G1-containing
46 ntained within aa 84 to 113 is a potentially arthritogenic epitope.
47                             Tenascin-C is an arthritogenic extracellular matrix glycoprotein that is
48                            Processing of the arthritogenic glycosylated CII(259-273) epitope, which i
49 ar processing of CII for presentation of the arthritogenic glycosylated epitope CII(259-273) to CD4 T
50 enerated antigenic CII fragments bearing the arthritogenic glycosylated epitope, 2) the antigenic CII
51  and keratan sulfate (KS) side chains of the arthritogenic human proteoglycans are removed.
52                       Here, we show that the arthritogenic Igs act through both Fc receptors (in part
53 tilage proteoglycan aggrecan, is immunogenic/arthritogenic in BALB/c mice.
54  observations demonstrate that fibrinogen is arthritogenic in mice and that the pathogenesis of FIA i
55 e acute Lyme arthritis by enhancing an acute arthritogenic inflammatory response initiated by spiroch
56 n is induced in C57BL/6J mice by transfer of arthritogenic K/BxN serum and allowed to resolve.
57 d with distinct protocols and volumes of the arthritogenic K/BxN serum, and periodontal bone damage.
58 und hyperproliferation of synovial cells and arthritogenic lymphocytes and heightened the production
59 deglycosylated appropriately, can be used as arthritogenic material in BALB/c mice.
60 in FcgammaRIII-driven production of critical arthritogenic mediators including IL-1beta and CXCL2.
61 ificantly reduced serum levels of a panel of arthritogenic mediators, including chemokines such as MI
62 cell, together with enhanced availability of arthritogenic microbial antigens caused by microbial per
63              Chikungunya virus (CHIKV) is an arthritogenic mosquito-transmitted alphavirus that is un
64 y Th2 (IL-4 and IL-10) cytokines whereas the arthritogenic mutant rCB10 induced predominantly Th1 (IF
65            Dominant T-cell recognition of an arthritogenic OspA epitope is one way in which the immun
66 mplex (MHC) binding sites of the immunogenic/arthritogenic p135H sequence.
67 t that an alternative complement-independent arthritogenic pathway could be operative in the absence
68    Our results suggest an alternative to the arthritogenic peptide hypothesis.
69 DR10 shows that there could even be a single arthritogenic peptide; we now suggest a possible consens
70 ricted immune responses to self-antigens, or arthritogenic peptides, might drive immunopathology.
71 d from future researches involving potential arthritogenic peptides.
72 th, rather than a predilection for selecting arthritogenic peptides.
73 eful in determining whether HLA-B27 presents arthritogenic peptides.
74 ity of HLA-B27 confers an ability to present arthritogenic peptides.
75 leles displaying a binding site for similar "arthritogenic" peptides.
76 D4+ T cells expressing a TCR specific for an arthritogenic PG epitope is sufficient to trigger sponta
77 - mice are a promising model to evaluate the arthritogenic potential of human autoAbs.
78 led to serve as an adjuvant in the immune or arthritogenic response to type II collagen in mice.
79                               However, their arthritogenic role remains undefined.
80 ually detectable synovitis after transfer of arthritogenic sera.
81 pleting mAb before and following transfer of arthritogenic serum and scored for clinical indications
82 e early inflammatory response to transferred arthritogenic serum from the K/BxN transgenic mouse.
83 ligand, lipopolysaccharide, concomitant with arthritogenic serum in IL-1 receptor-deficient mice resu
84  in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficien
85 either partial or complete protection in the arthritogenic serum transfer and the more aggressive gen
86 diated arthritis, induced by the transfer of arthritogenic serum.
87           Furthermore, B cells isolated from arthritogenic splenocytes treated in vitro with anti-IL-
88  this study we have shown that activation of arthritogenic splenocytes with antigen and agonistic ant
89                     Syngeneic fibroblasts or arthritogenic splenocytes, engineered to express tsCR1 u
90 hiMFV1 and the recently described phiMAV1 of arthritogenic strains of Mycoplasma arthritidis, along w
91                One of the cross-reactive and arthritogenic T cell epitopes (92GR/QVRVNSA/IY) is local
92                      The critical autoimmune/arthritogenic T cell epitopes of aggrecan are located in
93 ult proteoglycan inhibits the recognition of arthritogenic T cell epitopes, prevents the development
94      Fine epitope sequence recognition of an arthritogenic T cell hybridoma derived from p135H-primed
95 nique effects on priming of autoreactive and arthritogenic T cells, provides new insight for understa
96  mediating autoimmune arthritis, we isolated arthritogenic TCRs and characterized the self antigens t
97 s and differ from infections caused by other arthritogenic viruses, such as Ross River virus.

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