ライフサイエンスコーパス: lesional

1 Here we show that post-lesional AAV-assisted co-expression of two soluble prote

2 expression and function were investigated in lesional AD and psoriasis skin as well as in primary ker

3 antly, immune activation extends well beyond lesional AD because nonlesional skin and the blood compo

4 at neutrophilic inflammation is a feature of lesional AD pathology comorbid with allergic inflammatio

5 This is the first report of a lesional AD phenotype using RNA-seq and the first direct

6 Onset of lesional AD requires effective control of local and syst

7 P3 and caspase-1 expressions were reduced in lesional AD skin compared to psoriatic and healthy skin.

8 We sought to define the lesional AD transcriptome using RNA-seq and compare it u

9 y of the T-cell receptor (TCR) repertoire in lesional AD, and its relation to nonlesional skin remain

10 regulation of Cldn-4 in nonlesional, but not lesional, AD skin.

11 ormal skin, and was significantly greater in lesional ADEH+ skin than in lesional ADEH- skin.

12 antly greater in lesional ADEH+ skin than in lesional ADEH- skin.

13 formed microarray and RT-PCR profiling of 27 lesional and 17 nonlesional scalp samples from patients

14 sequencing of the beta-TCR repertoire in 29 lesional and 19 nonlesional AD biopsies, compared to six

15 As a result, we found peri-lesional and contralateral activations basically overlap

16 arametric classification was performed using lesional and global thresholds.

17 liative (seizure reduction) measure for both lesional and non-lesional forms of epilepsy.

18 e generated genome-wide expression data from lesional and non-lesional skin of chronic cutaneous LE (

19 s of P. acnes isolates recovered from paired lesional and non-lesional skin of PMH patients.

20 Nevertheless, both lesional and nonlesional AD showed a highly polyclonal T

21 t epidermal and dermal genomic signatures of lesional and nonlesional AD skin and normal skin compare

22 Lesional and nonlesional AD skin biopsies were collected

23 of the epidermal and dermal compartments of lesional and nonlesional AD skin compared with normal sk

24 try studies in baseline, week 2, and week 12 lesional and nonlesional biopsy specimens from 19 patien

25 xpression by immunohistochemical analysis of lesional and nonlesional cartilage from human and rodent

26 at DEPDC5 mutations are associated with both lesional and nonlesional epilepsies, even within the sam

27 the molecular and cellular skin pathology of lesional and nonlesional intrinsic AD and extrinsic AD b

28 Analysis of lesional and nonlesional skin biopsy specimens demonstra

29 Sequence analysis of DNA from lesional and nonlesional skin confirmed a BAP1 germline

30 We processed routine skin swabs from lesional and nonlesional skin from 40 patients with AD a

31 rmed to separate the epidermis and dermis of lesional and nonlesional skin from patients with AD and

32 l barrier functions, in normal skin and both lesional and nonlesional skin of patients with AD.

33 Genomic profiling of lesional and nonlesional skin of patients with atopic de

34 lated differentially expressed genes between lesional and nonlesional skin to the AD transcriptome.

35 , the sharing of top abundant clones between lesional and nonlesional skin, and their persistence aft

36 , including Th2/Th22 cells, are increased in lesional and nonlesional skin.

37 gnificantly from that in healthy controls in lesional and nonlesional skin.

38 AD, TCR repertoire diversity was similar in lesional and nonlesional tissues, and absolute numbers o

39 unch biopsy specimens from patients with HS (lesional and nonlesional) and healthy controls between O

40 ral myelin, axonal and dendrite integrity in lesional and normal-appearing tissue of the cortex and t

41 ge multiple sclerosis, their distribution in lesional and normal-appearing tissue, and their correlat

42 ared with remote from lesions (p = 0.007) or lesional and remote OA knee (p < 0.01) cartilage.

43 purified CD4+ and CD8+ T cells isolated from lesional and unaffected skin biopsies of psoriasis patie

44 patients affected with psoriasis, comparing lesional and unaffected skin.

45 ) and epidermal (thickness, K16) measures in lesional and, even more strongly, in nonlesional AD.

46 linical presentation and surgical outcome of lesional anterior cingulate epilepsy is possibly influen

47 y complex class 1-like molecule expressed in lesional aortic endothelial cells and macrophage-rich re

48 ed ultrasound, has again stirred interest in lesional approaches.In this article, we will discuss the

49 ed to a significant reduction in aortic root lesional area.

50 22, PI3/Elafin) correlated between blood and lesional as well as non-lesional skin.

51 Lesional, atrophy, and DT diffusion tensor MR measures o

52 s were taken from nonlesional (baseline) and lesional (baseline, days 1 and 3, and weeks 1, 2, 4, and

53 hat most of the 12 individuals studied had a lesional bias toward one side or the other, even showing

54 d) proteins were differentially expressed in lesional biopsy specimens from patients with AE relative

55 On lesional biopsy, a lichenoid infiltrate was observed in

56 trast material, we measured the evolution of lesional blood-brain barrier (BBB) permeability, compari

57 n that normobaric hyperoxia may benefit peri-lesional brain and white matter following traumatic brai

58 The stratum corneum of lesional but also clinically unaffected skin of adults w

59 g of AD, or SCORAD) are detected not only in lesional but also nonlesional skin and blood, more compl

60 with significant gene expression changes in lesional but also nonlesional skin, particularly reducti

61 Increased expression of CGRP and VEGF in lesional, but not uninvolved, skin indicates that these

62 In accord with our in vitro findings, lesional caspase 1 activity was abolished in P2X7(-/-) m

63 reduced expression of type 2 NO synthase by lesional CD11b(+) cells.

64 tors, whereas the mutation was restricted to lesional CD207(+) DC in low-risk LCH patients.

65 attributed to its impact on atherosclerotic lesional cells such as macrophages.

66 Here, we review how lesional cells undergo cell death and how failed clearan

67 Moreover, apoptosis of lesional cells was unaffected, and we found no evidence

68 ed twice weekly for 14 weeks, or until total lesional clearance was observed, whichever was earlier.

69 The reduction was greater in lesional compared with nonlesional skin.

70 s (94%), a single HPV type was found in each lesional component studied.

71 0.03; n = 7), nonlocalized (p < 0.001), and lesional cortical sites (p < 0.001) when compared to non

72 Lesional DCs from both types of CRSwNP produced enhanced

73 Blockade of OX40L and PD-L1 on lesional DCs from eosinophilic CRSwNP suppressed Th2 res

74 noneosinophilic CRSwNP, where OX40L/PD-L1(+) lesional DCs in eosinophilic CRSwNP could prime Th2 cell

75 ells, whereas the low OX40L/PD-L1-expressing lesional DCs in noneosinophilic CRSwNP primarily induced

76 The sorted lesional DCs were activated or cultured with autologous

77 Distinct subsets of lesional DCs were found in eosinophilic and noneosinophi

78 derangement of apoptosis and inflammation in lesional dendritic cells.

79 Despite a wide range of lesional doses being noted using fixed 100 mCi radioacti

80 tion imaging provides a better assessment of lesional dosimetry in contrast to traditional I-131 whol

81 sion: Routine use of WB/BC dosimetry without lesional dosimetry provided no OS advantage when compare

82 Routine use of WB/BC dosimetry without lesional dosimetry provided no OS advantage when compare

83 oid hormone, although the impact of reducing lesional dosimetry requires attention and further invest

84 onal oxidative stress and necrosis, improved lesional efferocytosis, and thicker fibrous caps.

85 ected, and we found no evidence of defective lesional efferocytosis.

86 no granulomas were observed and only single lesional eosinophils were detected, GPTD does not resemb

87 ive of reduced macrophage infiltration, less lesional expression of inducible nitric oxide synthase (

88 Expression of lesional FLAP in myeloid cells promotes leukotriene B(4)

89 reduction) measure for both lesional and non-lesional forms of epilepsy.

90 cortex that may be responsible for many 'non-lesional' forms of epilepsy.

91 The precise chain of events driving lesional granuloma formation has remained elusive for ma

92 y faster Go reaction times with their contra-lesional hand than the unoperated patients and did not d

93 ctive inhibition when tested with the contra-lesional hand.

94 ediates endothelial dysfunction and leads to lesional hemorrhage in diabetic human AR (hAR) expressin

95 Lesional HER2 status was verified by biopsies.

96 he granuloma has proven difficult because of lesional heterogeneity and the limitations of animal mod

97 Our data suggest that lesional heterogeneity arises, in part, through differen

98 esolved plaque inflammation by inhibition of lesional inflammasome activation and reduced experimenta

99 1; thoracic, P < 0.05; lumbar, P < 0.01) and lesional inflammation (border, P = 0.001; periplaque whi

100 entional candidate to attenuate dysregulated lesional inflammation and to restore functional recovery

101 reduces atherosclerosis without exaggerated lesional inflammation independent of metabolic risk fact

102 riant, autoantibody binding is followed by a lesional inflammatory cell infiltration, and the overall

103 th a significant increase in levels of intra-lesional inflammatory markers.

104 Here, we explore the role of lesional iron in multiple sclerosis using multiple appro

105 ll group 2D (NKG2D) ligand expression in the lesional keratinocytes associated with a marked CD4+ T c

106 follicular and follicular stratum corneum of lesional KP, which correlated ultrastructurally with imp

107 Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine.

108 uggesting that critical responses occur at a lesional level to ultimately determine the clinical outc

109 ts also attenuates the EMT signature even in lesional lichen planopilaris hair follicles ex vivo.

110 Therefore, we hypothesized that lesional lipid mediator imbalance favors atheroprogressi

111 tients with NOMID (n = 14) before treatment (lesional (LS) and non-lesional (pre-NL) skin) and after

112 that contributes to T cell recruitment into lesional lymph nodes in cHL.

113 d media and impaired in vivo following intra-lesional M2 cell depletion.

114 y of Cxcr7 increased neointima formation and lesional macrophage accumulation in hyperlipidemic mice

115 -26 reduces atherosclerotic lesion sizes and lesional macrophage accumulation.

116 2 key hallmarks of advanced atherosclerosis, lesional macrophage apoptosis and plaque necrosis, which

117 However, decreases in lesional macrophage content and remodeling in both group

118 lations of macrophages, the phenotype of the lesional macrophage is more complex and likely changes d

119 sses recent advances in our understanding of lesional macrophage phenotype and function in different

120 tes, although recent research has shown that lesional macrophage-like cells can also be derived from

121 deficiency reduced plaque size and number of lesional macrophages after partial carotid ligation in a

122 MitoOS in lesional macrophages amplifies atherosclerotic lesion de

123 ided with an increase in COX-2 expression in lesional macrophages and increased biosynthesis of throm

124 revealed that MC1-R expression localizes in lesional macrophages and is significantly associated wit

125 Lesional macrophages are derived primarily from blood mo

126 ptor class B1, and wound healing pathways in lesional macrophages during atherosclerosis regression.

127 crease in LRV1-induced disease severity, and lesional macrophages from these mice displayed reduced l

128 tion that circulating monocytes give rise to lesional macrophages has reinforced the concept that mon

129 CXCL9 expression in lesional macrophages implicates the skin as the source o

130 ges resulted in an increased total number of lesional macrophages in general and Ly6c(hi) infiltratin

131 Lesional macrophages in macaques and humans with tubercu

132 We demonstrate that lesional macrophages in WT mice express Axl but that Axl

133 ions and assessed the biological function of lesional macrophages isolated with laser-capture microdi

134 Lesional macrophages take on different phenotypes depend

135 MitoOS in lesional macrophages was successfully suppressed in thes

136 othelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switchi

137 nce of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defe

138 oxidative DNA damage, a marker of mitoOS in lesional macrophages, correlates with aortic root lesion

139 the increasing understanding of the roles of lesional macrophages, new research areas and treatment s

140 sclerosis by causing proliferation arrest of lesional macrophages, suggesting that drugs targeting ma

141 eading to an altered number and phenotype of lesional macrophages.

142 age correlated positively with the number of lesional macrophages.

143 ion by modulating the biological function of lesional macrophages.

144 ine atherosclerotic lesions, particularly by lesional macrophages.

145 01 [n=11], P=0.004) with a reduced amount of lesional macrophages.

146 plantation recurrence correlated with higher lesional maximum standardized uptake values: for PFS, P

147 At 5 years, lesional measures overtook magnetization transfer ratio

148 The averages of all lesional median values for TBF and (18)F-FAZA V(T) were

149 The decrease in lesional monocyte chemotactic protein-1 was associated w

150 The mechanism involves increased lesional monocyte recruitment associated with loss of Tr

151 Thus, imaging of lesional monocytes and macrophages could serve as a biom

152 xpression was also increased in inflammatory lesional morphea skin (fold change = 30.6, P = 0.006), a

153 transcriptional profiling of whole blood and lesional morphea skin, and used double-staining immunohi

154 Lesional myeloid cells were depleted and vascular smooth

155 and derive future directions for functional lesional neurosurgery, in particularly potential trial d

156 otropy decreased and mean diffusivity of non-lesional, normal-appearing white matter progressively in

157 lso compared with samples from patients with lesional or nonlesional AD and those with psoriasis.

158 cholesterol, hyperhomocysteinemia, increased lesional oxidative stress and adhesion molecule expressi

159 omotes plaque stability, including decreased lesional oxidative stress and necrosis, improved lesiona

160 ary outcomes were the differences in average lesional pain assessed by the Brief Pain Inventory and v

161 No significant difference in average lesional pain was observed between the study arms.

162 lesion mapping study investigating potential lesional patterns associated with headache in acute isch

163 R imaging to measure relative binding in the lesional, perilesional, and surrounding normal-appearing

164 dividuals, but the size of the right, contra-lesional planum temporale region may reflect a 'reserve

165 KC cultures grown from lesional (PP) and non-lesional (PN) biopsies of psoriasis patients and control

166 this caused a persistent suppression of the lesional pO2 and a concurrent increase of the parasite l

167 57BL/6 mice was paralleled by an increase of lesional pO2.

168 of primary monolayer KC cultures grown from lesional (PP) and non-lesional (PN) biopsies of psoriasi

169 14) before treatment (lesional (LS) and non-lesional (pre-NL) skin) and after treatment (post-NL) wi

170 e progression of advanced atherosclerosis or lesional processes associated with TAM receptor signalin

171 In lesional PRP skin samples from a single patient, upregul

172 L-17A) is the most abundant IL-17 isoform in lesional psoriasis skin (1058 versus 8 pg/ml; p < 0.006)

173 function for the elevated IL-17C observed in lesional psoriasis skin.

174 brodalumab treatment, with conversion of the lesional psoriasis transcriptome to resemble that seen i

175 ing (RNA-seq) to assay the transcriptomes of lesional psoriatic and normal skin.

176 nalysis of the p50 and c-Rel subunits within lesional psoriatic and systemic sclerosis skin revealed

177 In a transcriptome study of lesional psoriatic skin (PP) versus normal skin, we foun

178 a P2X7R variant that was highly expressed in lesional psoriatic skin compared with nonlesional psoria

179 creased presence of P2X7R in nonlesional and lesional psoriatic skin compared with normal healthy tis

180 p44+ ILC3 was significantly increased in non-lesional psoriatic skin compared with normal skin.

181 Furthermore, the strong IL-22 increase in lesional psoriatic skin was accompanied by a moderate in

182 Lesional psoriatic skin was analyzed by means of immunoh

183 layers of healthy skin epidermis, whereas in lesional psoriatic skin, it is reduced in the basal laye

184 -S100A9 and C3 are specifically expressed in lesional psoriatic skin.

185 TNF-alpha(+) cells or signs of apoptosis in lesional psoriatic skin.

186 ion is dysfunctional in both nonlesional and lesional psoriatic skin.

187 potentially important implications for post-lesional regenerative strategies in adults.

188 s had significantly higher histopathological lesional scores (for cumulative typhlitis index, inflamm

189 ally neutrophils, produced IL-17 at the skin lesional site.

190 nfiltrating immune cells expressed CXCL10 at lesional sites in skin of patients with BP.

191 DSS = 0) was observed in 16 (41%) psoriasis lesional sites treated with cyclosporine lipogel, 85.7%

192 age pool into peripheral blood (PB) to enter lesional sites, where most rapidly undergo apoptosis.

193 developed from separate, rather than initial lesional sites.

194 01; 95% CI, 13.77-24.51) in 59% of psoriasis lesional sites.

195 with HS, biopsy specimens were obtained from lesional skin (axilla or groin) and nonlesional skin.

196 e receptor 2 was shown to be activated in AD lesional skin (immediately proximal to the sweat ducts),

197 genes expressed in nonlesional (NLS-CSU) and lesional skin (LS-CSU) and peripheral blood were identif

198 iasis, we found that GRHL3 is upregulated in lesional skin and binds known epidermal differentiation

199 into proinflammatory Th17 cells occurring in lesional skin and blood of psoriasis patients.

200 rved in CGRP and VEGF expression between non-lesional skin and controls.

201 nous TLR4 ligands significantly elevated, in lesional skin and lung tissues from patients with sclero

202 LL37-specific T cells can infiltrate lesional skin and may be tracked in patients blood by te

203 To address this issue, we collected lesional skin biopsies from aGVHD (n = 25), clGVHD (n =

204 lated during activation, and are enriched in lesional skin biopsies from atopic patients.

205 nerves, mast cells, and the epidermis in the lesional skin biopsies from patients with AD, but not in

206 Higher expression of B7-H6 was observed in lesional skin biopsies of patients with atopic dermatiti

207 Lesional skin biopsy samples were taken from this patien

208 Lesional skin biopsy specimens and peripheral blood lymp

209 ave the c.49G>A, p.Glu17Lys AKT1 mutation in lesional skin but not in his blood.

210 In lesional skin children showed comparable or greater epid

211 bserved to be more abundant in the dermis of lesional skin from AD patients.

212 -like and inflammatory cells in SSc skin and lesional skin from mice in the bleomycin (bleo)-induced

213 long noncoding RNA (lncRNA) transcriptome in lesional skin from psoriasis patients before (PP) and af

214 sease hallmarks (keratin 16 and loricrin) in lesional skin from responders (P < .05).

215 analysis revealed upregulation of CD200R in lesional skin from subjects with an extrinsic AD phenoty

216 mma-induced chemokine CXCL10 is expressed in lesional skin from vitiligo patients, and that it is cri

217 treatment resulted in reduced expression of lesional skin genes associated with IL-23/IL-17 signalin

218 Lesional skin in CSU contained significantly more CGRP+

219 gulator of the transition from uninvolved to lesional skin in psoriasis.

220 ease in the cutaneous nerve fiber density in lesional skin in vivo.

221 athologic epidermal alterations in psoriatic lesional skin include increased epidermal expression of

222 In lesional skin keratinocyte pSTAT1 and pSTAT3 staining wa

223 itiligo, including decreased circulating and lesional skin levels of alpha-melanocyte-stimulating hor

224 Thousands of aberrantly expressed genes in lesional skin normalized within 2 weeks following brodal

225 e-wide expression data from lesional and non-lesional skin of chronic cutaneous LE (CCLE) patients.

226 es reflected an IFN-alpha-signature, whereas lesional skin of exanthemas showed induction of TH2-asso

227 ned the outcome of sensitization through non-lesional skin of individuals with AD and healthy control

228 d in the lungs of asthma patients and in the lesional skin of individuals with atopic dermatitis, whe

229 cyte infiltrates with IgA in cryosections of lesional skin of patients suffering from this disease.

230 phylococcus aureus (S. aureus) isolates from lesional skin of patients with AD, produced a substantia

231 on is increased in keratinocytes and chronic lesional skin of patients with AD.

232 Activated T cells in lesional skin of patients with atopic dermatitis (AD) an

233 keratin 16, Mki67, and S100A7/A8/A9) defined lesional skin of patients with both variants.

234 of miR-146a and miR-146b (miR-146a/b) in the lesional skin of patients with psoriasis.

235 n CD8(+) T cells isolated from the blood and lesional skin of patients with SSc with severe skin thic

236 expression of IFN-gamma is increased in the lesional skin of patients, however, it is currently unkn

237 lates recovered from paired lesional and non-lesional skin of PMH patients.

238 tivating ligands reduced inflammation in the lesional skin of psoriasis patients, whereas AhR antagon

239 ns of filaggrin and human beta-defensin 2 in lesional skin of these patients were markedly reduced.

240 Moreover, regulatory T cells in lesional skin played an important role in disease remiss

241 ffected skin, while sorted CD8+ T cells from lesional skin produced higher levels of IL-17, IL-22, IF

242 Sorted CD4+ T cells from psoriatic lesional skin produced higher levels of IL-17A, IL-22, a

243 cytokines and matrix-degrading proteases in lesional skin samples confirmed the clinical suspicion o

244 From 1 patient, lesional skin samples were taken before ustekinumab trea

245 nd a reduced epidermal hyperproliferation at lesional skin sites.

246 atients and the recruitment of Treg cells in lesional skin support the interest of promoting Treg cel

247 from normal-appearing skin to posttreatment lesional skin to active skin lesions in patients with AD

248 (AD) models link epidermal abnormalities in lesional skin to cytokine activation.

249 There is a 26% overlap of the blood and lesional skin transcriptional profile from a previous an

250 1 in the upper and lower epidermal layers of lesional skin was detected.

251 yses showed the numbers of neutrophils in AD lesional skin were comparable with those in psoriatic le

252 esions compared with matched biopsies of non-lesional skin when the following criteria were applied:

253 colonized with Staphylococcus aureus in the lesional skin whereas most healthy individuals do not ha

254 penetration not only in intact, but also in lesional skin with impaired skin barrier function is imp

255 at correlates gene expression fold change in lesional skin with the Psoriasis Area and Severity Index

256 skin were comparable with those in psoriatic lesional skin, and both were correlated with the extent

257 e IL-17 ligand genes that are upregulated in lesional skin, IL17A, IL17C, and IL17F, were all downreg

258 In lesional skin, microbiome types consisted predominantly

259 margination in the upper stratum spinosum in lesional skin, suggesting impaired intercellular adhesio

260 In lesional skin, VEGF and CGRP co-localised to UEA-1+ bloo

261 increased levels of histamine are present in lesional skin, we investigated the effect of histamine,

262 and KRT85) were significantly suppressed in lesional skin.

263 ficantly more CGRP+ and VEGF+ cells than non-lesional skin.

264 cytokines, levels of which are increased in lesional skin.

265 ed between blood and lesional as well as non-lesional skin.

266 ected skin of psoriasis patients compared to lesional skin.

267 ytokines and other inflammatory mediators in lesional skin.

268 ntly of myeloid origin, infiltrate psoriatic lesional skin.

269 ges, and origins and phenotypic switching of lesional smooth muscle cells.

270 Lesional standardized uptake values were calculated, as

271 t TLA (r = 0.60, P = 0.0005) but not highest lesional SUV(max) of each scan.

272 Lesion quantity, mean and maximum lesional SUV, z score, and percentage of affected bone v

273 eligible for this study and had collected a lesional swab for polymerase chain reaction (PCR).

274 al assessment, syphilis serology, and PCR on lesional swabs to detect the presence of T pallidum pert

275 mplications of HLA-C*06:02 and mechanisms of lesional T cell activation in psoriasis, however, remain

276 erogenic T cell-derived interferon-gamma and lesional T cell infiltration, and was abrogated in CD4(+

277 Lesional T cells responded to tofacitinib with reduced p

278 nt vessel wall inflammation is maintained by lesional T cells, including the newly identified tissue-

279 Most (87%) top expanded lesional T-cell clones were shared with nonlesional tiss

280 Cortical lesional T2* was compared with patients' normal-appearin

281 ecognition that host immunopathology affects lesional TB drug distribution means that pharmacokinetic

282 c type surgical specimens into normal versus lesional tissue and low-grade versus high-grade tumors w

283 capacity, CD57+ T cells are less frequent in lesional tissue due to the high cellular turnover.

284 of high levels of hypophosphorylated NRF2 in lesional tissue.

285 The DD treponemes were isolated from lesional tissues but not from control feet or other area

286 under the cornoid lamella of PMVK-deficient lesional tissues, with incomplete differentiation of ker

287 argets and the unsolved problem of bilateral lesional treatment.

288 onsistency, efficacy and side effect rate of lesional treatments for tremor are presented separately

289 moattractant protein-1 (MCP-1) and 36% lower lesional vascular cell adhesion molecule-1 (VCAM-1).

290 h recovery period results in augmentation of lesional vascularity and perfusion, as well as improved

291 , >/= 2.0; false discovery rate </= 0.05) in lesional versus nonlesional skin from 18 patients with m

292 Lesional vessels did not express GLUT1 or the lymphatic

293 ed an original algorithm to cluster adjacent lesional voxels (cluxels) in each subject and tested whe

294 greater T-cell infiltrates were observed in lesional vs nonlesional AD, TCR repertoire diversity was

295 We established the AA transcriptomes (lesional vs nonlesional: 734 DEGs [297 upregulated and 4

296 EGs [297 upregulated and 437 downregulated]; lesional vs normal: 4230 DEGs [1980 upregulated and 2250

297 n was significantly down-regulated in paired lesional vs. macroscopically normal cartilage samples fr

298 ified as differentially expressed (psoriatic lesional vs. psoriatic non-lesional) was found using sta

299 ressed (psoriatic lesional vs. psoriatic non-lesional) was found using statistical and fold-change cu

300 ue in MS multiple sclerosis , whereas global lesional, WM white matter , and GM gray matter damage do