ライフサイエンスコーパス: Lyme arthritis

1 rmed the contribution of type I IFN genes to Lyme arthritis.

2 n in chronic, antibiotic treatment-resistant Lyme arthritis.

3 the spectrum of the severity and duration of Lyme arthritis.

4 ents with facial palsy and 68% of those with Lyme arthritis.

5 t correlate with the severity or duration of Lyme arthritis.

6 sb as a transgene were protected from severe Lyme arthritis.

7 R2 prevented the development of experimental Lyme arthritis.

8 uirement for the development of experimental Lyme arthritis.

9 in triggering antibiotic treatment-resistant Lyme arthritis.

10 mice and correlated with the development of Lyme arthritis.

11 lecules in patients with treatment-resistant Lyme arthritis.

12 een identified that regulate the severity of Lyme arthritis.

13 agocytic cells and the development of murine Lyme arthritis.

14 l in the pathogenesis of treatment-resistant Lyme arthritis.

15 sons with untreated and antibiotic-resistant Lyme arthritis.

16 d in the pathogenesis of treatment-resistant Lyme arthritis.

17 rthritis induced by Borrelia burgdorferi, or Lyme arthritis.

18 ed intensely in the synovia of patients with Lyme arthritis.

19 uction in untreated and antibiotic-resistant Lyme arthritis.

20 s a target for immune-mediated resolution of Lyme arthritis.

21 ates the inflammatory events associated with Lyme arthritis.

22 ontrast, IL-11 blocking antibodies increased Lyme arthritis.

23 responsible for these two manifestations of Lyme arthritis.

24 resistance or susceptibility to experimental Lyme arthritis.

25 t-responsive and 16 with treatment-resistant Lyme arthritis.

26 which may contribute to the pathogenesis of Lyme arthritis.

27 i results in the development of experimental Lyme arthritis.

28 rime initiator of PMN migration during acute Lyme arthritis.

29 ved from synovial fluid of two patients with Lyme arthritis.

30 w that CD4 T cell responses influence murine Lyme arthritis.

31 tients and in the synovium of 1 patient with Lyme arthritis.

32 erved in the synovial fluid of patients with Lyme arthritis.

33 g patients representative of the spectrum of Lyme arthritis.

34 eN-scid mice increased the severity of acute Lyme arthritis.

35 L-8 is involved in the pathogenesis of acute Lyme arthritis.

36 lly for the induction of severe, destructive Lyme arthritis.

37 nfection in mice determine susceptibility to Lyme arthritis.

38 in determining the severity of acute murine Lyme arthritis.

39 ibute to the joint pathology associated with Lyme arthritis.

40 s of three patients with treatment-resistant Lyme arthritis.

41 direct, effector role in the pathogenesis of Lyme arthritis.

42 hese three patients with treatment-resistant Lyme arthritis.

43 vel virulence factor and a trigger of murine Lyme arthritis.

44 ted spirochetes induced a severe destructive Lyme arthritis.

45 d in the pathogenesis of treatment-resistant Lyme arthritis.

46 ri are directly involved in the induction of Lyme arthritis.

47 te to the development of treatment-resistant Lyme arthritis.

48 a reduction in the severity of acute murine Lyme arthritis.

49 cA have been noted in American patients with Lyme arthritis.

50 mononuclear cells (PBMCs) from patients with Lyme arthritis.

51 and may contribute to antibiotic-refractory Lyme arthritis.

52 to the development of antibiotic-refractory Lyme arthritis.

53 cells and patients with erythema migrans or Lyme arthritis.

54 nterferon (IFN) in the development of murine Lyme arthritis.

55 s and subsequent development of experimental Lyme arthritis.

56 ction in patients with antibiotic-refractory Lyme arthritis.

57 eri genotypes in the joints of patients with Lyme arthritis.

58 role for this cytokine in the development of Lyme arthritis.

59 ility or resistance to antibiotic-refractory Lyme arthritis.

60 nation of B. burgdorferi and pathogenesis of Lyme arthritis.

61 ly, the progression to antibiotic-refractory Lyme arthritis.

62 y response to infection in a murine model of Lyme arthritis.

63 suggest new strategies for the treatment of Lyme arthritis.

64 in altered joint inflammation during murine Lyme arthritis.

65 of Bb-infected CD28-/- mice develop chronic Lyme arthritis.

66 on, only very rarely presenting with chronic Lyme arthritis.

67 ese mice only after establishment of chronic Lyme arthritis.

68 provide a murine model for studying chronic Lyme arthritis.

69 mokines and cytokines in the pathogenesis of Lyme arthritis.

70 ay be involved in regulating the severity of Lyme arthritis.

71 tion of aggrecanases to joint destruction in Lyme arthritis.

72 n who had erythema migrans, facial palsy, or Lyme arthritis 10-20 years ago and 30 uninfected control

73 verity of joint swelling and the duration of Lyme arthritis after antibiotic treatment are associated

74 flammation may persist in some patients with Lyme arthritis after the apparent eradication of the spi

75 r the presence of 1 or 2 treatment-resistant Lyme arthritis alleles were 0.8 (95% confidence interval

76 Treatment-resistant Lyme arthritis alleles were not found more commonly in p

77 from 17 patients with antibiotic-responsive Lyme arthritis and 35 patients with antibiotic-refractor

78 found in synovial fluids from patients with Lyme arthritis and are induced from cartilage tissue by

79 subset accumulate in synovial fluid of human Lyme arthritis and are intensely cytolytic toward a wide

80 These cells are restricted to patients with Lyme arthritis and are localized to the joint.

81 ences in the inflammatory infiltrates during Lyme arthritis and carditis and demonstrate the coexiste

82 dant role in the development of experimental Lyme arthritis and carditis via CXCR2-mediated recruitme

83 molecules play a role in the development of Lyme arthritis and carditis.

84 tibiotic-refractory or antibiotic-responsive Lyme arthritis and correlated these frequencies with in

85 patients with antibiotic treatment-resistant Lyme arthritis and from 10 control subjects were tested

86 ri and the HGE agent on the course of murine Lyme arthritis and granulocytic ehrlichiosis.

87 unable to modulate the development of severe Lyme arthritis and had no effect on spirochete clearance

88 ules in 29 patients with treatment-resistant Lyme arthritis and in 15 patients with rheumatoid arthri

89 ) and MMP-3 have been found in patients with Lyme arthritis and in in vitro models of Lyme arthritis

90 eased in patients with antibiotic-refractory Lyme arthritis and in those with post-treatment Lyme dis

91 1 (B6.C3-Bbaa1), which developed more severe Lyme arthritis and K/BxN model of rheumatoid arthritis (

92 ecules is a marker for antibiotic-refractory Lyme arthritis and might play a role in the pathogenesis

93 data also suggest that antibiotic-refractory Lyme arthritis and post-treatment Lyme disease syndrome

94 nvolved in the regulation of the severity of Lyme arthritis and predict the involvement of regulatory

95 lta1 subset accumulate in inflamed joints in Lyme arthritis and proliferate in response to stimulatio

96 or blocking mAb reduced the severity of both Lyme arthritis and RA in B6.C3-Bbaa1 mice, formally link

97 e additional evidence of a role for IL-17 in Lyme arthritis and reveal an additional regulatory targe

98 a contributing factor in the development of Lyme arthritis and show that its production and histopat

99 vial fluid samples from patients with active Lyme arthritis and were elevated in the joints of mice i

100 1+ individuals to the development of chronic Lyme arthritis and, eventually, the progression to antib

101 s, synovial fluid samples from patients with Lyme arthritis, and cartilage tissue from Lyme arthritis

102 d in the pathogenesis of treatment-resistant Lyme arthritis, and epitope contained within aa 84 to 11

103 vial fluid samples from patients with active Lyme arthritis, and in the joints of mice by real-time q

104 Early Lyme disease, Lyme arthritis, and neuroborreliosis may respond just as

105 es, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.

106 a migrans (EM), joint fluid of patients with Lyme arthritis, and supernatants of Borrelia burgdorferi

107 ogenesis of the inflammatory process seen in Lyme arthritis, and that Th2 cells modulate the pro-infl

108 entified in the joint fluid of patients with Lyme arthritis, and the genotype frequencies found in jo

109 ry responses were amplified in patients with Lyme arthritis, and the highest responses were observed

110 multiple sclerosis; Borrelia burgdorfii and Lyme arthritis; and B4 Coxsackievirus, cytomegalovirus o

111 The cause and pathogenesis of Lyme arthritis are complex.

112 usceptibility to development of experimental Lyme arthritis are mediated by the innate immune respons

113 biotic-responsive, or non-antibiotic-treated Lyme arthritis as an indirect measure of spirochetal per

114 resistant to the development of experimental Lyme arthritis as measured by ankle swelling and arthrit

115 Individuals with treatment-resistant Lyme arthritis, but not other forms of arthritis, genera

116 ivity was not necessary for the induction of Lyme arthritis, but that its deficiency resulted in earl

117 genotypes were not as great in patients with Lyme arthritis, but those infected with RST1 strains mor

118 Vitamin A deficiency may exacerbate acute Lyme arthritis by enhancing an acute arthritogenic infla

119 ese results contrasted with the reduction of Lyme arthritis by IL-12 antibodies in immunocompetent an

120 Lyme arthritis can histologically resemble rheumatoid sy

121 Lyme arthritis, caused by the spirochete Borrelia burgdo

122 h cells from synovial fluid of patients with Lyme arthritis coexpressed IL-17 and TNF-alpha upon poly

123 s and found that only American patients with Lyme arthritis commonly had antibody responses to OspA,

124 sed levels of both pathogens and more severe Lyme arthritis compared with those in mice infected with

125 , there was no difference in the severity of Lyme arthritis compared with wild type controls, followi

126 ynovial fluid lymphocytes from patients with Lyme arthritis contain a large proportion of gamma delta

127 , patients with chronic, treatment-resistant Lyme arthritis develop an immune response against OspA,

128 o an infected joint is a key requirement for Lyme arthritis development and that altered recruitment

129 ckade revealed a unique role for IFN-beta in Lyme arthritis development in B6.C3-Bbaa1 mice.

130 sultant type I IFN induction associated with Lyme arthritis development may involve multiple triggeri

131 gs further tie early type I IFN induction to Lyme arthritis development, a connection not previously

132 viously unappreciated role for type I IFN in Lyme arthritis development.

133 In addition, the severity of Lyme arthritis directly correlates with the ratio of Th1

134 Borrelia burgdorferi, the causative agent of Lyme arthritis, does not produce any exported proteases

135 xposed antigen, is a major trigger of murine Lyme arthritis; even in cases of larger challenge inocul

136 , and 33% (11 of 33) of the individuals with Lyme arthritis had P21 antibodies, suggesting that a P21

137 Genetic susceptibility to murine Lyme arthritis has been correlated with the dominance of

138 The development of experimental Lyme arthritis has been correlated with the expression o

139 e patients, their role in the development of Lyme arthritis has not been determined.

140 The role of aggrecanases in Lyme arthritis has not yet been determined.

141 better understanding of the pathogenesis of Lyme arthritis has provided clues about the mechanisms r

142 esistance and susceptibility to experimental Lyme arthritis have been linked with the production of i

143 Patients with antibiotic-refractory Lyme arthritis have high synovial fluid levels of proinf

144 Studies in patients with chronic Lyme arthritis have indicated that an autoimmune process

145 e pathogenic mechanisms that sustain chronic Lyme arthritis have not been fully elucidated, although

146 netic predisposition to treatment-refractory Lyme arthritis, HLA-DR transgenic mice have been used.

147 a dose-dependent increase in the severity of Lyme arthritis in C3H/HeN mice.

148 ze eicosanoid production during experimental Lyme arthritis in mice infected with the bacterium Borre

149 ated with pregnancy can alter the outcome of Lyme arthritis in mice.

150 Inhibition of myostatin in vivo suppressed Lyme arthritis in the reduced interval Bbaa1 congenic mi

151 e root of the differential susceptibility to Lyme arthritis in these two strains of mice.

152 y foster susceptibility to diseases, such as Lyme arthritis, in which activated macrophage and inflam

153 igens in patients with antibiotic-refractory Lyme arthritis, in which infection-induced autoimmunity

154 B. burgdorferi was grown) and controls (non-Lyme arthritis inflammatory joint disease, syphilis, mul

155 Thus, the majority of patients with Lyme arthritis initially have increased frequencies of O

156 Antibiotic treatment-resistant Lyme arthritis is a chronic inflammatory joint disease t

157 Treatment-resistant Lyme arthritis is associated with immune reactivity to o

158 murine Lyme borreliosis because experimental Lyme arthritis is dependent, at least partially, upon th

159 The mechanism(s) by which Lyme arthritis is induced has not been elucidated.

160 Lyme arthritis is initiated by the tick-borne spirochete

161 esistance to the development of experimental Lyme arthritis is maintained.

162 esion molecules in synovium in patients with Lyme arthritis is surely critical in the control of Borr

163 Lyme arthritis is the most common complication following

164 0 (IL-10) and IL-12 (cytokines implicated in Lyme arthritis), it is necessary for host control of cer

165 Using cartilage explant models of Lyme arthritis, it appeared that the cleavage of aggreca

166 in synovial fluid (SF) from 63 patients with Lyme arthritis (LA) and in synovial tissue from 9 patien

167 Lyme arthritis (LA) can usually be prevented by early tr

168 es in patients with erythema migrans (EM) or Lyme arthritis (LA) to elucidate their role early and la

169 discover novel autoantigens associated with Lyme arthritis (LA), we identified T-cell epitopes prese

170 Differences between human and murine Lyme arthritis may be related to the lack of induction o

171 he TCR repertoire of fresh synovial fluid in Lyme arthritis may represent more a synovium-tropic or n

172 may underlie differences in the severity of Lyme arthritis observed in the patient population and su

173 Treatment-resistant Lyme arthritis occurs in a subset of Lyme arthritis pati

174 Patients with antibiotic-refractory Lyme arthritis often have lower frequencies of Treg cell

175 8 deficiency did not abrogate development of Lyme arthritis or carditis.

176 Conversely, vitamin A may lessen acute Lyme arthritis pathology by blocking IFN-gamma and IL-12

177 )-2 has been implicated in the regulation of Lyme arthritis pathology, and subsequent lipidomic profi

178 ant Lyme arthritis (TRLA) develops in 10% of Lyme arthritis patients and is characterized by continuo

179 sistant Lyme arthritis occurs in a subset of Lyme arthritis patients and is linked to HLA.DRB1*0401 (

180 omedullin in the synovial fluid of untreated Lyme arthritis patients was elevated compared with that

181 lasma cells from the joint tissue of chronic Lyme arthritis patients who underwent synovectomy.

182 Treatment-resistant Lyme arthritis patients' T cells, cloned based on their

183 ltrating T cells in synovial fluid from nine Lyme arthritis patients, before and after stimulation wi

184 Consistent with observations in chronic Lyme arthritis patients, the infected mutant, but not wi

185 Chronic Lyme arthritis persisting even after antibiotic treatmen

186 vitis in patients with antibiotic-refractory Lyme arthritis persists for months to several years afte

187 and mice displaying different severities of Lyme arthritis possess different alleles of the OPN gene

188 e immunologic events that lead to persistent Lyme arthritis post-antibiotic therapy in genetically su

189 joint inflammation in certain patients with Lyme arthritis post-antibiotic treatment have been elusi

190 important role in regulating inflammation in Lyme arthritis, potentially through the cleavage of type

191 from five patients with treatment-resistant Lyme arthritis preferentially recognized Borrelia burgdo

192 emale C3H mice consistently developed severe Lyme arthritis, pregnant mice had a marked reduction in

193 cted throughout infection from the joints of Lyme arthritis-resistant and -susceptible mice and subje

194 of MMPs were significantly lower in the more Lyme arthritis-resistant BALB/c and C57BL/6 mice.

195 5-LOX(-/-)) mice, which display a failure of Lyme arthritis resolution, recruited fewer F4/80(+) cell

196 In contrast, patients whose Lyme arthritis resolves within 3 months postinfection sh

197 Lyme arthritis results from colonization of joints by Bo

198 s and 35 patients with antibiotic-refractory Lyme arthritis seen during the past 18 years.

199 i-associated locus 1 (Bbaa1), that regulates Lyme arthritis severity and includes the 15 type I IFN g

200 ix metalloproteinase 9, a known modulator of Lyme arthritis severity.

201 Thus, models of Lyme arthritis should include the possible contribution

202 ith prolonged antibiotic treatment-resistant Lyme arthritis, suggesting the possibility of an autoimm

203 th Lyme arthritis, and cartilage tissue from Lyme arthritis-susceptible and -resistant mice by using

204 After infection of Lyme arthritis-susceptible C3H/HeJ mice with Borrelia bu

205 In Lyme arthritis synovia, endothelial cells showed intense

206 Lyme arthritis synovial fluid contains a large proportio

207 a burgdorferi, synovial Vdelta1 T cells from Lyme arthritis synovial fluid potently induce maturation

208 I IFN has been uniquely linked to the severe Lyme arthritis that develops in C3H mice infected with t

209 (-/-) mice develop intermittent monarticular Lyme arthritis that is responsive to antibiotics.

210 sly been shown between antibiotic-refractory Lyme arthritis, the human histocompatibility leukocyte a

211 In a murine model of antibiotic-refractory Lyme arthritis, the numbers of Treg cells are dramatical

212 Although mice are a well-accepted model for Lyme arthritis, there are significant differences compar

213 the current study, we used a murine model of Lyme arthritis to investigate the role 5-LO products mig

214 Treatment-resistant Lyme arthritis (TRLA) develops in 10% of Lyme arthritis

215 ith Lyme arthritis and in in vitro models of Lyme arthritis using cartilage explants and chondrocytes

216 We developed an in vitro model of Lyme arthritis using cartilage explants and observed cha

217 lls in six patients with treatment-resistant Lyme arthritis, using an HLA-DRB1*0401 major histocompat

218 Synovial fluid from patients with Lyme arthritis was found to contain at least 3 MMPs: gel

219 The development and resolution of Lyme arthritis was similar in transgenic and nontransgen

220 Lyme arthritis was studied in IL-6-deficient mice, since

221 active cells involved in the propagation of Lyme arthritis we have utilized intracellular cytokine s

222 Using a mouse model of Lyme arthritis, we demonstrate that CD14 deficiency lead

223 sess the role of FasL in the pathogenesis of Lyme arthritis, we evaluated the response to B. burgdorf

224 e of NK cells in development of experimental Lyme arthritis, we examined their activation in vivo in

225 eri proteins that may have a role in chronic Lyme arthritis, we studied the natural history of the an

226 nt for this lipoprotein in the generation of Lyme arthritis, we utilized targeted deletion to generat

227 response to infection and the development of Lyme arthritis were identified by global gene expression

228 When PBMCs from patients with Lyme arthritis were stimulated with a B burgdorferi RST1

229 0 patients with other arthritides, including Lyme arthritis, were negative.

230 The 26 patients with Lyme arthritis, who had received antibiotic therapy for