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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
7 isease signs in mice infected with a related arthritogenic alphavirus, Ross River virus, but not in m
9 of new expression vectors for two Old World arthritogenic alphaviruses (Sindbis and Chikungunya viru
13 hritic infiltrates seen after infection with arthritogenic alphaviruses such as chikungunya virus.
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
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
28 /c mice expressing a TCR that recognizes the arthritogenic ATEGRVRVNSAYQDK peptide of human cartilage
31 ction as antigen-presenting cells (APCs) for arthritogenic autoantigens found within inflamed joint t
37 une signals, including TLR4 agonists and the arthritogenic cytokine, IL-1beta, via an NFkappaB pathwa
40 nal antibody therapy that aborted lethal and arthritogenic disease in wild-type and immunocompromised
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
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
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
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
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
64 y Th2 (IL-4 and IL-10) cytokines whereas the arthritogenic mutant rCB10 induced predominantly Th1 (IF
67 t that an alternative complement-independent arthritogenic pathway could be operative in the absence
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.
76 D4+ T cells expressing a TCR specific for an arthritogenic PG epitope is sufficient to trigger sponta
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
88 this study we have shown that activation of arthritogenic splenocytes with antigen and agonistic ant
90 hiMFV1 and the recently described phiMAV1 of arthritogenic strains of Mycoplasma arthritidis, along w
93 ult proteoglycan inhibits the recognition of arthritogenic T cell epitopes, prevents the development
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
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