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1 ot cause B. burgdorferi 25015 to become more arthritogenic.
2 lting mutant rCB10T614P,A617E product became arthritogenic.
3 esulting mutant CB8P449T,E452A was no longer arthritogenic.
5 a faecal bacterial strain that has exhibited arthritogenic activity in animal models and that favours
6 esponses to stimulation with a citrullinated arthritogenic aggrecan peptide were detected in RA patie
9 rthritis and polyarthralgia is a hallmark of arthritogenic alphavirus infections, with an exceptional
11 Furthermore, due to the explosive nature of arthritogenic alphavirus outbreaks and their recent expa
15 isease signs in mice infected with a related arthritogenic alphavirus, Ross River virus, but not in m
18 of new expression vectors for two Old World arthritogenic alphaviruses (Sindbis and Chikungunya viru
21 ing antibodies that protect against multiple arthritogenic alphaviruses are elicited during natural i
24 in a manner that is similar to the way that arthritogenic alphaviruses bind to the structurally unre
28 gs shed light on how preexisting immunity to arthritogenic alphaviruses may affect secondary infectio
31 hritic infiltrates seen after infection with arthritogenic alphaviruses such as chikungunya virus.
34 a member of a globally distributed group of arthritogenic alphaviruses that cause weeks to months of
36 ments or vaccines are not available for most arthritogenic alphaviruses, and recently licensed vaccin
37 d Irf1 (-/-) mice with two distantly related arthritogenic alphaviruses, chikungunya virus (CHIKV) an
38 -1 in modulating pathogenesis of two related arthritogenic alphaviruses, chikungunya virus and Ross R
40 es the tropism and pathogenesis for multiple arthritogenic alphaviruses, including chikungunya virus
41 butes to control of RRV infection.IMPORTANCE Arthritogenic alphaviruses, including Ross River virus (
44 ied receptor for several clinically relevant arthritogenic alphaviruses, its detailed role in the cel
46 understanding of the transmission cycles of arthritogenic alphaviruses, their vectors, epidemiology,
49 eactive antibodies that protect against both arthritogenic and encephalitic alphaviruses have not bee
51 e antiviral activity of mouse Ifitm3 against arthritogenic and encephalitic alphaviruses using cells
54 1A(low) T cells were tissue-invasive and pro-arthritogenic, and MRE11A reconstitution mitigated synov
55 itiate disease by helping B cells to produce arthritogenic anti-glucose-6-phosphate isomerase (anti-G
56 is and is induced by well-defined monoclonal arthritogenic antibodies and enhanced by injection of li
57 ital imaging to demonstrate that transfer of arthritogenic antibodies caused macromolecular vasoperme
59 /c mice expressing a TCR that recognizes the arthritogenic ATEGRVRVNSAYQDK peptide of human cartilage
63 ction as antigen-presenting cells (APCs) for arthritogenic autoantigens found within inflamed joint t
68 is (RA); however, their specific role in key arthritogenic cells such as the synovial fibroblast (SF)
69 .315 protects mice against infection by both arthritogenic (chikungunya and Mayaro) and encephalitic
72 une signals, including TLR4 agonists and the arthritogenic cytokine, IL-1beta, via an NFkappaB pathwa
77 nal antibody therapy that aborted lethal and arthritogenic disease in wild-type and immunocompromised
80 at causes acute, subacute, and chronic human arthritogenic diseases and, in rare instances, can lead
81 tion of HCG was initiated 2 days prior to an arthritogenic dose of streptococcal cell wall (SCW) in n
82 W (3 microg/day), initiated 7 days before an arthritogenic dose of systemic SCW, virtually eliminated
83 in normal adult articular cartilage, and the arthritogenic epitope(s) remains intact in G1-containing
87 ar processing of CII for presentation of the arthritogenic glycosylated epitope CII(259-273) to CD4 T
88 enerated antigenic CII fragments bearing the arthritogenic glycosylated epitope, 2) the antigenic CII
92 observations demonstrate that fibrinogen is arthritogenic in mice and that the pathogenesis of FIA i
93 e acute Lyme arthritis by enhancing an acute arthritogenic inflammatory response initiated by spiroch
96 d with distinct protocols and volumes of the arthritogenic K/BxN serum, and periodontal bone damage.
97 und hyperproliferation of synovial cells and arthritogenic lymphocytes and heightened the production
99 in FcgammaRIII-driven production of critical arthritogenic mediators including IL-1beta and CXCL2.
100 ificantly reduced serum levels of a panel of arthritogenic mediators, including chemokines such as MI
101 cell, together with enhanced availability of arthritogenic microbial antigens caused by microbial per
103 y Th2 (IL-4 and IL-10) cytokines whereas the arthritogenic mutant rCB10 induced predominantly Th1 (IF
108 t that an alternative complement-independent arthritogenic pathway could be operative in the absence
110 DR10 shows that there could even be a single arthritogenic peptide; we now suggest a possible consens
111 ricted immune responses to self-antigens, or arthritogenic peptides, might drive immunopathology.
117 D4+ T cells expressing a TCR specific for an arthritogenic PG epitope is sufficient to trigger sponta
119 SKG CD4 T cells marked their autoreactivity, arthritogenic potential, and ability to more readily dif
120 led to serve as an adjuvant in the immune or arthritogenic response to type II collagen in mice.
123 pleting mAb before and following transfer of arthritogenic serum and scored for clinical indications
124 e early inflammatory response to transferred arthritogenic serum from the K/BxN transgenic mouse.
125 ligand, lipopolysaccharide, concomitant with arthritogenic serum in IL-1 receptor-deficient mice resu
126 in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficien
127 either partial or complete protection in the arthritogenic serum transfer and the more aggressive gen
130 this study we have shown that activation of arthritogenic splenocytes with antigen and agonistic ant
133 hiMFV1 and the recently described phiMAV1 of arthritogenic strains of Mycoplasma arthritidis, along w
134 r sequencing (scTCR-Seq) to profile a highly arthritogenic subset of naive CD4+ T cells from BALB/c-Z
138 ult proteoglycan inhibits the recognition of arthritogenic T cell epitopes, prevents the development
139 Fine epitope sequence recognition of an arthritogenic T cell hybridoma derived from p135H-primed
140 nique effects on priming of autoreactive and arthritogenic T cells, provides new insight for understa
141 mediating autoimmune arthritis, we isolated arthritogenic TCRs and characterized the self antigens t