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1 te has been killed (known as post-infectious Lyme arthritis).
2 urgdorferi results in prolonged nonresolving Lyme arthritis.
3 ence of regulatory T cells and recovery from Lyme arthritis.
4 on, only very rarely presenting with chronic Lyme arthritis.
5 ese mice only after establishment of chronic Lyme arthritis.
6 provide a murine model for studying chronic Lyme arthritis.
7 mokines and cytokines in the pathogenesis of Lyme arthritis.
8 ay be involved in regulating the severity of Lyme arthritis.
9 tion of aggrecanases to joint destruction in Lyme arthritis.
10 n in chronic, antibiotic treatment-resistant Lyme arthritis.
11 the spectrum of the severity and duration of Lyme arthritis.
12 rmed the contribution of type I IFN genes to Lyme arthritis.
13 ents with facial palsy and 68% of those with Lyme arthritis.
14 t correlate with the severity or duration of Lyme arthritis.
15 R2 prevented the development of experimental Lyme arthritis.
16 uirement for the development of experimental Lyme arthritis.
17 in triggering antibiotic treatment-resistant Lyme arthritis.
18 mice and correlated with the development of Lyme arthritis.
19 lecules in patients with treatment-resistant Lyme arthritis.
20 een identified that regulate the severity of Lyme arthritis.
21 agocytic cells and the development of murine Lyme arthritis.
22 l in the pathogenesis of treatment-resistant Lyme arthritis.
23 sons with untreated and antibiotic-resistant Lyme arthritis.
24 d in the pathogenesis of treatment-resistant Lyme arthritis.
25 rthritis induced by Borrelia burgdorferi, or Lyme arthritis.
26 ed intensely in the synovia of patients with Lyme arthritis.
27 uction in untreated and antibiotic-resistant Lyme arthritis.
28 s a target for immune-mediated resolution of Lyme arthritis.
29 role for this cytokine in the development of Lyme arthritis.
30 ates the inflammatory events associated with Lyme arthritis.
31 ontrast, IL-11 blocking antibodies increased Lyme arthritis.
32 responsible for these two manifestations of Lyme arthritis.
33 resistance or susceptibility to experimental Lyme arthritis.
34 t-responsive and 16 with treatment-resistant Lyme arthritis.
35 i results in the development of experimental Lyme arthritis.
36 rime initiator of PMN migration during acute Lyme arthritis.
37 ved from synovial fluid of two patients with Lyme arthritis.
38 w that CD4 T cell responses influence murine Lyme arthritis.
39 in altered joint inflammation during murine Lyme arthritis.
40 tients and in the synovium of 1 patient with Lyme arthritis.
41 g patients representative of the spectrum of Lyme arthritis.
42 eN-scid mice increased the severity of acute Lyme arthritis.
43 L-8 is involved in the pathogenesis of acute Lyme arthritis.
44 lly for the induction of severe, destructive Lyme arthritis.
45 nfection in mice determine susceptibility to Lyme arthritis.
46 in determining the severity of acute murine Lyme arthritis.
47 ibute to the joint pathology associated with Lyme arthritis.
48 s of three patients with treatment-resistant Lyme arthritis.
49 direct, effector role in the pathogenesis of Lyme arthritis.
50 hese three patients with treatment-resistant Lyme arthritis.
51 ted spirochetes induced a severe destructive Lyme arthritis.
52 d in the pathogenesis of treatment-resistant Lyme arthritis.
53 ri are directly involved in the induction of Lyme arthritis.
54 te to the development of treatment-resistant Lyme arthritis.
55 sb as a transgene were protected from severe Lyme arthritis.
56 a reduction in the severity of acute murine Lyme arthritis.
57 test; P < 0.0001) relative to subjects with Lyme arthritis.
58 is of postinfectious (antibiotic-refractory) Lyme arthritis.
59 ages, whereas IgG3/IgG1/IgG4 was enriched in Lyme arthritis.
60 which may contribute to the pathogenesis of Lyme arthritis.
61 erved in the synovial fluid of patients with Lyme arthritis.
62 vel virulence factor and a trigger of murine Lyme arthritis.
63 cA have been noted in American patients with Lyme arthritis.
64 mononuclear cells (PBMCs) from patients with Lyme arthritis.
65 and may contribute to antibiotic-refractory Lyme arthritis.
66 to the development of antibiotic-refractory Lyme arthritis.
67 cells and patients with erythema migrans or Lyme arthritis.
68 nterferon (IFN) in the development of murine Lyme arthritis.
69 s and subsequent development of experimental Lyme arthritis.
70 ction in patients with antibiotic-refractory Lyme arthritis.
71 eri genotypes in the joints of patients with Lyme arthritis.
72 ility or resistance to antibiotic-refractory Lyme arthritis.
73 nation of B. burgdorferi and pathogenesis of Lyme arthritis.
74 ly, the progression to antibiotic-refractory Lyme arthritis.
75 y response to infection in a murine model of Lyme arthritis.
76 suggest new strategies for the treatment of Lyme arthritis.
77 of Bb-infected CD28-/- mice develop chronic Lyme arthritis.
78 n who had erythema migrans, facial palsy, or Lyme arthritis 10-20 years ago and 30 uninfected control
79 verity of joint swelling and the duration of Lyme arthritis after antibiotic treatment are associated
80 flammation may persist in some patients with Lyme arthritis after the apparent eradication of the spi
81 r the presence of 1 or 2 treatment-resistant Lyme arthritis alleles were 0.8 (95% confidence interval
83 from 17 patients with antibiotic-responsive Lyme arthritis and 35 patients with antibiotic-refractor
84 found in synovial fluids from patients with Lyme arthritis and are induced from cartilage tissue by
85 subset accumulate in synovial fluid of human Lyme arthritis and are intensely cytolytic toward a wide
87 ences in the inflammatory infiltrates during Lyme arthritis and carditis and demonstrate the coexiste
88 dant role in the development of experimental Lyme arthritis and carditis via CXCR2-mediated recruitme
90 tibiotic-refractory or antibiotic-responsive Lyme arthritis and correlated these frequencies with in
91 patients with antibiotic treatment-resistant Lyme arthritis and from 10 control subjects were tested
93 unable to modulate the development of severe Lyme arthritis and had no effect on spirochete clearance
94 ules in 29 patients with treatment-resistant Lyme arthritis and in 15 patients with rheumatoid arthri
95 ) and MMP-3 have been found in patients with Lyme arthritis and in in vitro models of Lyme arthritis
96 eased in patients with antibiotic-refractory Lyme arthritis and in those with post-treatment Lyme dis
97 1 (B6.C3-Bbaa1), which developed more severe Lyme arthritis and K/BxN model of rheumatoid arthritis (
99 ecules is a marker for antibiotic-refractory Lyme arthritis and might play a role in the pathogenesis
100 data also suggest that antibiotic-refractory Lyme arthritis and post-treatment Lyme disease syndrome
101 d its 2 main adverse outcomes-postinfectious Lyme arthritis and posttreatment Lyme disease syndrome-a
102 nvolved in the regulation of the severity of Lyme arthritis and predict the involvement of regulatory
103 lta1 subset accumulate in inflamed joints in Lyme arthritis and proliferate in response to stimulatio
104 or blocking mAb reduced the severity of both Lyme arthritis and RA in B6.C3-Bbaa1 mice, formally link
105 e additional evidence of a role for IL-17 in Lyme arthritis and reveal an additional regulatory targe
106 a contributing factor in the development of Lyme arthritis and show that its production and histopat
107 vial fluid samples from patients with active Lyme arthritis and were elevated in the joints of mice i
108 1+ individuals to the development of chronic Lyme arthritis and, eventually, the progression to antib
109 s, synovial fluid samples from patients with Lyme arthritis, and cartilage tissue from Lyme arthritis
110 d in the pathogenesis of treatment-resistant Lyme arthritis, and epitope contained within aa 84 to 11
111 vial fluid samples from patients with active Lyme arthritis, and in the joints of mice by real-time q
113 es, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.
114 - and convalescent-phase early Lyme disease, Lyme arthritis, and posttreatment Lyme disease syndrome,
115 a migrans (EM), joint fluid of patients with Lyme arthritis, and supernatants of Borrelia burgdorferi
116 ogenesis of the inflammatory process seen in Lyme arthritis, and that Th2 cells modulate the pro-infl
117 entified in the joint fluid of patients with Lyme arthritis, and the genotype frequencies found in jo
118 ry responses were amplified in patients with Lyme arthritis, and the highest responses were observed
119 multiple sclerosis; Borrelia burgdorfii and Lyme arthritis; and B4 Coxsackievirus, cytomegalovirus o
121 usceptibility to development of experimental Lyme arthritis are mediated by the innate immune respons
124 biotic-responsive, or non-antibiotic-treated Lyme arthritis as an indirect measure of spirochetal per
125 resistant to the development of experimental Lyme arthritis as measured by ankle swelling and arthrit
127 ivity was not necessary for the induction of Lyme arthritis, but that its deficiency resulted in earl
128 genotypes were not as great in patients with Lyme arthritis, but those infected with RST1 strains mor
129 Vitamin A deficiency may exacerbate acute Lyme arthritis by enhancing an acute arthritogenic infla
130 ese results contrasted with the reduction of Lyme arthritis by IL-12 antibodies in immunocompetent an
133 mice, BLT1(-/-) mice developed nonresolving Lyme arthritis characterized by increased neutrophils in
134 h cells from synovial fluid of patients with Lyme arthritis coexpressed IL-17 and TNF-alpha upon poly
135 s and found that only American patients with Lyme arthritis commonly had antibody responses to OspA,
136 sed levels of both pathogens and more severe Lyme arthritis compared with those in mice infected with
137 , there was no difference in the severity of Lyme arthritis compared with wild type controls, followi
138 ynovial fluid lymphocytes from patients with Lyme arthritis contain a large proportion of gamma delta
139 , patients with chronic, treatment-resistant Lyme arthritis develop an immune response against OspA,
140 o an infected joint is a key requirement for Lyme arthritis development and that altered recruitment
142 sultant type I IFN induction associated with Lyme arthritis development may involve multiple triggeri
143 gs further tie early type I IFN induction to Lyme arthritis development, a connection not previously
146 Borrelia burgdorferi, the causative agent of Lyme arthritis, does not produce any exported proteases
147 xposed antigen, is a major trigger of murine Lyme arthritis; even in cases of larger challenge inocul
148 understanding of the pathogenetic events in Lyme arthritis, from initial infection in the skin, thro
149 , and 33% (11 of 33) of the individuals with Lyme arthritis had P21 antibodies, suggesting that a P21
154 better understanding of the pathogenesis of Lyme arthritis has provided clues about the mechanisms r
155 esistance and susceptibility to experimental Lyme arthritis have been linked with the production of i
158 e pathogenic mechanisms that sustain chronic Lyme arthritis have not been fully elucidated, although
159 netic predisposition to treatment-refractory Lyme arthritis, HLA-DR transgenic mice have been used.
161 ze eicosanoid production during experimental Lyme arthritis in mice infected with the bacterium Borre
163 ease with a sensitivity of 48.5% and 75% and Lyme arthritis in serum from patients with Lyme arthriti
164 Inhibition of myostatin in vivo suppressed Lyme arthritis in the reduced interval Bbaa1 congenic mi
166 y foster susceptibility to diseases, such as Lyme arthritis, in which activated macrophage and inflam
167 igens in patients with antibiotic-refractory Lyme arthritis, in which infection-induced autoimmunity
168 B. burgdorferi was grown) and controls (non-Lyme arthritis inflammatory joint disease, syphilis, mul
173 murine Lyme borreliosis because experimental Lyme arthritis is dependent, at least partially, upon th
177 esion molecules in synovium in patients with Lyme arthritis is surely critical in the control of Borr
179 0 (IL-10) and IL-12 (cytokines implicated in Lyme arthritis), it is necessary for host control of cer
181 in synovial fluid (SF) from 63 patients with Lyme arthritis (LA) and in synovial tissue from 9 patien
185 es in patients with erythema migrans (EM) or Lyme arthritis (LA) to elucidate their role early and la
187 discover novel autoantigens associated with Lyme arthritis (LA), we identified T-cell epitopes prese
192 he TCR repertoire of fresh synovial fluid in Lyme arthritis may represent more a synovium-tropic or n
193 may underlie differences in the severity of Lyme arthritis observed in the patient population and su
195 y reported that patients with postinfectious Lyme arthritis often harbor the peptidoglycan (PG) cell
199 )-2 has been implicated in the regulation of Lyme arthritis pathology, and subsequent lipidomic profi
200 from a synovial gammadelta T cell clone of a Lyme arthritis patient and observed that it stains monoc
202 ant Lyme arthritis (TRLA) develops in 10% of Lyme arthritis patients and is characterized by continuo
203 sistant Lyme arthritis occurs in a subset of Lyme arthritis patients and is linked to HLA.DRB1*0401 (
204 omedullin in the synovial fluid of untreated Lyme arthritis patients was elevated compared with that
207 ltrating T cells in synovial fluid from nine Lyme arthritis patients, before and after stimulation wi
208 Consistent with observations in chronic Lyme arthritis patients, the infected mutant, but not wi
210 vitis in patients with antibiotic-refractory Lyme arthritis persists for months to several years afte
211 and mice displaying different severities of Lyme arthritis possess different alleles of the OPN gene
212 e immunologic events that lead to persistent Lyme arthritis post-antibiotic therapy in genetically su
213 joint inflammation in certain patients with Lyme arthritis post-antibiotic treatment have been elusi
214 important role in regulating inflammation in Lyme arthritis, potentially through the cleavage of type
215 from five patients with treatment-resistant Lyme arthritis preferentially recognized Borrelia burgdo
216 emale C3H mice consistently developed severe Lyme arthritis, pregnant mice had a marked reduction in
218 cted throughout infection from the joints of Lyme arthritis-resistant and -susceptible mice and subje
220 5-LOX(-/-)) mice, which display a failure of Lyme arthritis resolution, recruited fewer F4/80(+) cell
224 i-associated locus 1 (Bbaa1), that regulates Lyme arthritis severity and includes the 15 type I IFN g
227 ith prolonged antibiotic treatment-resistant Lyme arthritis, suggesting the possibility of an autoimm
229 th Lyme arthritis, and cartilage tissue from Lyme arthritis-susceptible and -resistant mice by using
233 a burgdorferi, synovial Vdelta1 T cells from Lyme arthritis synovial fluid potently induce maturation
234 I IFN has been uniquely linked to the severe Lyme arthritis that develops in C3H mice infected with t
236 sly been shown between antibiotic-refractory Lyme arthritis, the human histocompatibility leukocyte a
237 In a murine model of antibiotic-refractory Lyme arthritis, the numbers of Treg cells are dramatical
238 I, 83% to 100%) for serum from patients with Lyme arthritis; the STT algorithm detected early Lyme di
239 Although mice are a well-accepted model for Lyme arthritis, there are significant differences compar
240 solution of inflammation during experimental Lyme arthritis through the activation of PPAR-gamma.
241 the current study, we used a murine model of Lyme arthritis to investigate the role 5-LO products mig
243 ith Lyme arthritis and in in vitro models of Lyme arthritis using cartilage explants and chondrocytes
245 lls in six patients with treatment-resistant Lyme arthritis, using an HLA-DRB1*0401 major histocompat
249 active cells involved in the propagation of Lyme arthritis we have utilized intracellular cytokine s
251 sess the role of FasL in the pathogenesis of Lyme arthritis, we evaluated the response to B. burgdorf
252 e of NK cells in development of experimental Lyme arthritis, we examined their activation in vivo in
253 eri proteins that may have a role in chronic Lyme arthritis, we studied the natural history of the an
254 nt for this lipoprotein in the generation of Lyme arthritis, we utilized targeted deletion to generat
255 response to infection and the development of Lyme arthritis were identified by global gene expression
260 d Lyme arthritis in serum from patients with Lyme arthritis with a sensitivity of 100%, and the speci