ライフサイエンスコーパス: lupus

1 us) but not mineral oil (MO) (do not develop lupus).

2 or anti-phospholipid antibodies, promote CNS lupus.

3 lap with inflammatory processes in cutaneous lupus.

4 is critical for pathological B cell cues in lupus.

5 otential for therapeutic benefit in treating lupus.

6 cal value of targeting this pathway in human lupus.

7 her this process is altered in patients with lupus.

8 his cytokine promotes autoimmunity in murine lupus.

9 C1q deficiency could affect pristane-induced lupus.

10 accumulation of IgG-ICs in human and murine lupus.

11 and type I IFN responses in a mouse model of lupus.

12 mpen the pathogenic autoantibody response in lupus.

13 ethal autoimmune disease in a mouse model of lupus.

14 of this process in autoantibody secretion in lupus.

15 sion of disease in the NZB/W murine model of lupus.

16 tieres syndrome (AGS) and familial chilblain lupus.

17 results in aberrant Ab production resembling lupus.

18 T cells (TFH cells) occurs in patients with lupus.

19 referred to as central nervous system (CNS) lupus.

20 apoptotic cell clearance in human and murine lupus.

21 estraining autoreactive B cell activation in lupus.

22 ay promote the resolution of inflammation in lupus and infectious diseases.

23 8a, which occurs frequently in patients with lupus and lupus-prone mice, facilitated the development

24 nhibitor of NF-kappaB1 (ABIN1) predispose to lupus and other autoimmune diseases in at least eight hu

25 offer new opportunities for the treatment of lupus and other autoimmune diseases.

26 matory connective tissue diseases (CTD) like lupus and rheumatoid arthritis associate with cardiovasc

27 cal treatment of autoimmune diseases such as lupus and rheumatoid arthritis.

28 bodies, and systemic autoimmunity resembling lupus and Sjogren syndrome.

29 r results with B6.lpr mice, another model of lupus, and showed that a continuous treatment is require

30 I, fibrinogen, lipoprotein(a), homocysteine, lupus anticoagulant, anticardiolipin antibodies and geno

31 he clotting test is used in the diagnosis of lupus anticoagulants.

32 ma and IL-17A/F, further implicating SHP2 in lupus-associated immunopathology.

33 Thus, lupus-associated inflammation disrupts the blood-brain b

34 A cell-penetrating, anti-DNA, lupus autoantibody, 3E10, was previously shown to inhibi

35 vely regulates Th17 cell differentiation and lupus autoimmunity.

36 was upregulated in activated human and mouse lupus B cells, leading to prevention of disease developm

37 in mice treated i.p. with pristane (develop lupus) but not mineral oil (MO) (do not develop lupus).

38 as mediators of peripheral tissue damage in lupus, but it remains unclear whether they influence los

39 aimed at targeting B cells in patients with lupus by blocking BAFF, type I interferon, or TLR7 to TL

40 l treatment, consistent with the findings in lupus CD4(+)T cells.

41 CNS lupus typically presents at lupus diagnosis or within the first year, suggesting tha

42 cytes in brain tissue, which correlates with lupus disease and limited neuropathology.

43 dulator in clinical development for systemic lupus erythematosis and relapsed/refractory multiple mye

44 6.7%]), psoriasis (18 [20.9%]), and systemic lupus erythematosus (12 [14.0%]) were the most common au

45 ng (aHR, 1.9; 95% CI, 1.1-3.4), and systemic lupus erythematosus (aHR, 3.5, 95% CI, 1.1-11).

46 Systemic lupus erythematosus (lupus) is characterized by autoanti

47 e correlation with neuropsychiatric systemic lupus erythematosus (NPSLE) symptoms.

48 n C1q deficiency is associated with systemic lupus erythematosus (SLE) and increased susceptibility t

49 Patients with systemic lupus erythematosus (SLE) and primary Sjogren's syndrome

50 gen in autoimmune disorders such as systemic lupus erythematosus (SLE) and Sjogren's syndrome (SS).

51 and IL-23 receptor in patients with systemic lupus erythematosus (SLE) as compared with healthy contr

52 to be the major IFNalpha source in systemic lupus erythematosus (SLE) but their phenotype and functi

53 T cells from patients with systemic lupus erythematosus (SLE) display a number of abnormalit

54 Systemic lupus erythematosus (SLE) has a strong but incompletely

55 Patients with systemic lupus erythematosus (SLE) have accelerated cardiovascula

56 Numerous risk alleles for systemic lupus erythematosus (SLE) have now been identified.

57 Systemic lupus erythematosus (SLE) is a chronic, life-threatening

58 Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune

59 Systemic lupus erythematosus (SLE) is a known risk factor for end

60 Systemic lupus erythematosus (SLE) is a multi-organ autoimmune di

61 Systemic lupus erythematosus (SLE) is a prototypic autoimmune dis

62 Systemic lupus erythematosus (SLE) is an autoimmune disease with

63 Systemic lupus erythematosus (SLE) is an autoimmune disorder char

64 Systemic lupus erythematosus (SLE) is an incurable autoimmune dis

65 Systemic lupus erythematosus (SLE) is characterized by aberrant T

66 Systemic lupus erythematosus (SLE) is characterized by both conti

67 is involved in the pathogenesis of systemic lupus erythematosus (SLE) is unclear.

68 ion-based studies have been done on systemic lupus erythematosus (SLE) mortality trends in the United

69 D33/LAIR-1 expression is reduced in systemic lupus erythematosus (SLE) myelomonocytes.

70 eater coagulant effects compared to systemic lupus erythematosus (SLE) non APS IgG.

71 autoimmune response reminiscent of systemic lupus erythematosus (SLE) occurs in its absence.

72 12.31 was replicated in a cohort of systemic lupus erythematosus (SLE) patients (N = 47) and controls

73 ity landscape of naive B cells from Systemic Lupus Erythematosus (SLE) patients undergoing disease fl

74 ve been found to be associated with systemic lupus erythematosus (SLE) susceptibility by a recent gen

75 come of 39 variants associated with Systemic Lupus Erythematosus (SLE) through the integration of GWA

76 ncy (CVID), Evans syndrome (ES), or systemic lupus erythematosus (SLE), and most achieved a CR (N = 8

77 sis in autoimmune diseases, such as systemic lupus erythematosus (SLE), but the natural history of au

78 tical role in autoimmunity, such as systemic lupus erythematosus (SLE), by helping B cells.

79 nesis of autoimmunity, most notably systemic lupus erythematosus (SLE), diabetes mellitus, and dermat

80 Here we found that in human systemic lupus erythematosus (SLE), IgE antibodies specific for d

81 In systemic lupus erythematosus (SLE), many self-antigens are found

82 eral autoimmune diseases, including systemic lupus erythematosus (SLE), Sjogren's syndrome, inflammat

83 nked to autoimmune diseases such as systemic lupus erythematosus (SLE), where nucleic acid-containing

84 choroidal changes in patients with systemic lupus erythematosus (SLE), with or without glomeruloneph

85 glomerulonephritis, which resembled systemic lupus erythematosus (SLE)-like autoimmune disease.

86 lls (LysM(Cre)Bim(fl/fl)) develop a systemic lupus erythematosus (SLE)-like disease that mirrors aged

87 dies for diagnosis and prognosis of Systemic Lupus Erythematosus (SLE).

88 nd 11 patients with well-controlled systemic lupus erythematosus (SLE).

89 ephritis, a serious complication of systemic lupus erythematosus (SLE).

90 cleoli, are pathogenic hallmarks of systemic lupus erythematosus (SLE).

91 cus-specific association testing in systemic lupus erythematosus (SLE).

92 r implicated in the pathogenesis of systemic lupus erythematosus (SLE).

93 he comprehensive care of women with systemic lupus erythematosus (SLE).

94 s with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE).

95 and chromatin drive autoimmunity in systemic lupus erythematosus (SLE).

96 sed to underlie the pathogenesis of systemic lupus erythematosus (SLE).

97 fer risk for the autoimmune disease systemic lupus erythematosus (SLE).

98 inst nuclear Ags is the hallmark of systemic lupus erythematosus (SLE).

99 b) strongly associate with risk for systemic lupus erythematosus (SLE).

100 d with autoimmune diseases, such as systemic lupus erythematosus (SLE).

101 ers in spontaneous murine models of systemic lupus erythematosus (SLE).

102 ts are associated with the risk for systemic lupus erythematosus (SLE); however, it is unclear how Ox

103 in the inflammation associated with systemic lupus erythematosus (SLE); however, it remains unclear w

104 and total creatine, correlate with systemic lupus erythematosus activity.

105 ydroxychloroquine used for treating systemic lupus erythematosus and a Syk inhibitor blocked NA-TLR l

106 remarkable for an aunt who died of systemic lupus erythematosus and for a brother with arthritis.

107 nhibitory pathways in two systemic (systemic lupus erythematosus and rheumatoid arthritis) and two or

108 y of autoimmune diseases, including systemic lupus erythematosus and rheumatoid arthritis.

109 appa may play a pathogenic role in cutaneous lupus erythematosus and serve as a target for treatment.

110 B cells play an important role in systemic lupus erythematosus by acting not only as precursors of

111 usion values from all patients with systemic lupus erythematosus correlated positively with systemic

112 ematosus correlated positively with systemic lupus erythematosus disease activity index score (P = 0.

113 Patients with systemic lupus erythematosus exhibit accelerated atherosclerosis,

114 D cells obtained from patients with systemic lupus erythematosus exhibited increased CD45 activity an

115 Cutaneous lupus erythematosus is a disfiguring and common manifest

116 Systemic lupus erythematosus is an autoimmune disease that can af

117 Evaluation of discoid and subacute cutaneous lupus erythematosus lesions showed significant epidermal

118 -driven autoimmune diseases such as systemic lupus erythematosus or psoriasis, but pDCs are also invo

119 Lupus erythematosus patients suffer from elevated EBV lo

120 Because systemic lupus erythematosus patients were shown to acquire autoa

121 About a third of systemic lupus erythematosus patients, however, lack the IFN sign

122 SHP-1 axis function in B cells from systemic lupus erythematosus patients.

123 more advanced disease did not alter systemic lupus erythematosus progression.

124 Basophils from patients with systemic lupus erythematosus show an activated phenotype, correla

125 ients with rheumatoid arthritis and systemic lupus erythematosus were demethylated compared to health

126 tions in the brain of patients with systemic lupus erythematosus with and without a history of centra

127 corpus callosum of 13 patients with systemic lupus erythematosus with past NPSLE, 16 patients with sy

128 In patients with systemic lupus erythematosus with past NPSLE, significantly highe

129 ons were made between patients with systemic lupus erythematosus with/without past NPSLE and healthy

130 s with past NPSLE, 16 patients with systemic lupus erythematosus without past NPSLE, and 19 healthy c

131 e and patient type (with vs without systemic lupus erythematosus).

132 tibodies that are characteristic of systemic lupus erythematosus, a chronic autoimmune disease with m

133 ed with autoimmune diseases such as systemic lupus erythematosus, Aicardi-Goutieres syndrome (AGS) an

134 examined B cells from patients with systemic lupus erythematosus, an autoimmune disorder with a stron

135 s atherosclerosis, type-2 diabetes, systemic lupus erythematosus, and rheumatoid arthritis.

136 ic anemia (AA), autoimmune uveitis, systemic lupus erythematosus, and sickle cell disease, respective

137 iguring and common manifestation in systemic lupus erythematosus, and the etiology of this predisposi

138 icardi-Goutieres syndrome (AGS) and systemic lupus erythematosus, can arise when TREX1 function is co

139 In systemic lupus erythematosus, deposits of IgG-immune complexes an

140 a diverse array of diseases such as systemic lupus erythematosus, diabetes, and cancer.

141 y of human rheumatoid arthritis and systemic lupus erythematosus, indicating that increased autophagy

142 ated with type I diabetes mellitus, systemic lupus erythematosus, RA, and celiac disease, these resul

143 between SJS/TEN and pre-existing depression, lupus erythematosus, recent pneumonia, chronic kidney di

144 es, and autoimmune disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis).

145 urrent and future impact of AMDs on systemic lupus erythematosus, rheumatoid arthritis, and devastati

146 immune connective tissue disorders: systemic lupus erythematosus, rheumatoid arthritis, systemic scle

147 s, such as rheumatoid arthritis and systemic lupus erythematosus, show a polygenic inheritance patter

148 Using an inducible model of systemic lupus erythematosus, we found that passive transfer of a

149 d model of autoimmunity, similar to systemic lupus erythematosus, where both cell types are critical

150 f the most severe manifestations of systemic lupus erythematosus, with considerable morbidity and mor

151 sm for its increased production in cutaneous lupus erythematosus.

152 y be a viable therapeutic target in systemic lupus erythematosus.

153 sis, inflammatory bowel disease and systemic lupus erythematosus.

154 e use of BAFF-targeted therapies in systemic lupus erythematosus.

155 ound in AA, autoimmune uveitis, and systemic lupus erythematosus.

156 hy individuals and in patients with systemic lupus erythematosus.

157 classic mouse model of spontaneous systemic lupus erythematosus.

158 ablasts/PCs in patients with active systemic lupus erythematosus.

159 of intracellular innate sensors in systemic lupus erythematosus.

160 ciated disease in a murine model of systemic lupus erythematosus.

161 stic of autoimmune diseases such as systemic lupus erythematosus.

162 n CD4(+) T cells from patients with systemic lupus erythematosus.

163 ldhood and are also associated with systemic lupus erythematosus.

164 granulocytes from individuals with systemic lupus erythematosus.

165 ymorphisms that are associated with systemic lupus erythematosus.

166 utoantibody-driven diseases such as systemic lupus erythematosus.

167 scular/autoimmune disorders such as systemic lupus erythematosus; lymphoproliferative disorders such

168 the most serious manifestations of systemic lupus erythematous (SLE).

169 The domestic dog (Canis lupus familiaris) has been used in biomedical research f

170 A high-salt diet markedly increased lupus features in MRL/lpr mice.

171 chloroquine has been in use in patients with lupus for more than 50 years, but oligonucleotide-based

172 despite showing promise in animal models of lupus, have not reached the primary end point in a recen

173 negative Proteobacteria and known inducer of lupus in mice, into the circulation.

174 erences may contribute to the development of lupus in these mice.

175 against cancer, inflammation, arthritis, and lupus in vivo.

176 nts for the main aspects of human and murine lupus including the expansion of DN T cells, decreased I

177 ctivity in the MRL/lpr and NZB/NZW models of lupus, inhibiting multiple pathogenic responses.

178 hallmark of autoimmunity in murine models of lupus is the formation of germinal centers (GCs) in lymp

179 Systemic lupus erythematosus (lupus) is characterized by autoantibody-mediated organ i

180 Thus, lupus keratinocytes are primed for IL-6 hyperproduction

181 Increased production of IFN-kappa by lupus keratinocytes drives this response, indicating tha

182 er toll-like receptor 2 and UVB treatment in lupus keratinocytes, and neutralization of IFN-kappa dec

183 e I IFN blockade decreased IL-6 secretion by lupus keratinocytes.

184 on of IFN-kappa decreased IL-6 production by lupus keratinocytes.

185 clear dying cells and the establishment of a lupus-like autoimmune disease in mice.

186 to bacterial superantigens may precipitate a lupus-like autoimmune disease through activation of DNT

187 ral killer (NK) cell function and promotes a lupus-like autoimmune disease.

188 results demonstrate that, in the setting of lupus-like CD4 T cell-driven B cell hyperactivity, IL-21

189 prime repair exonuclease 1 (TREX1) cause the lupus-like disease Aicardi-Goutieres syndrome in which a

190 staphylococcal enterotoxin B precipitated a lupus-like inflammatory disease with characteristic lymp

191 raperitoneal injection of pristane induces a lupus-like syndrome whose pathogenesis implicates the se

192 in cooperatively breeding grey wolves (Canis lupus Linnaeus 1758).

193 wn that CD4(+) T cells from B6.Sle1Sle2.Sle3 lupus mice and patients present a high cellular metaboli

194 igration and alleviated clinical symptoms in lupus mice.

195 In a type I IFN-accelerated lupus model, treatment with an antagonist Ox40:Fc fusion

196 f the IFN-alpha driving autoimmunity in this lupus model.

197 eceptor (TLR) ligands is prominent in murine lupus models and some bacterial infections, but the inhi

198 liferative GN (HR, 0.84; 95% CI, 0.76-0.92), lupus nephritis (HR, 0.69; 95% CI, 0.66-0.71), vasculiti

199 Management of patient with Lupus Nephritis (LN) continues to remain a challenge for

200 Lupus nephritis (LN) is a potentially dangerous end orga

201 d-derived cells is a key pathogenic event in lupus nephritis (LN), but the process is poorly understo

202 IgAN, for those with secondary GN subtypes: lupus nephritis [HR,0.91; 95% CI, 0.86-0.97], vasculitis

203 of profibrotic markers in animal models with lupus nephritis and folic acid nephropathy.

204 what we know about processes that may cause lupus nephritis and how such basic processes may be affe

205 ment of drugs to prevent, and perhaps treat, lupus nephritis and other autoinflammatory diseases caus

206 ce elevated autoantibody levels and promoted lupus nephritis by inducing BAFF production in the kidne

207 AFF plays a previously unappreciated role in lupus nephritis by inducing renal TLSs and regulating th

208 New Zealand White) F1 (NZB/W) mouse model of lupus nephritis compared with healthy New Zealand White

209 A previous study of anti-C1q in experimental lupus nephritis demonstrated an important role for Fcgam

210 they age and succumb to a disease resembling lupus nephritis in humans.

211 ular and humoral autoimmune responses during lupus nephritis in NZB/W F1 mice and emphasize the poten

212 ee themes, the pathogenic role of T cells in lupus nephritis is not clear.

213 Compared with samples from patients with lupus nephritis or healthy black controls, AASK-N sample

214 promise to improve upon the standard-of-care lupus nephritis treatments.

215 Treatment of lupus nephritis urine samples with 0.5% acetic acid prod

216 IL-23R(-/-)MRL.lpr mice displayed attenuated lupus nephritis with a striking decrease in the accumula

217 tasis have been identified as biomarkers for lupus nephritis, a serious complication of systemic lupu

218 r disease entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and additional features as

219 oved survival in patients with proliferative lupus nephritis, and combined administration of these ag

220 e glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.

221 of complement activation in dermatomyositis, lupus nephritis, and necrotic muscle fibres in Duchenne

222 anous nephropathy, membranoproliferative GN, lupus nephritis, and vasculitis associated with HRs (95%

223 e discuss current therapeutic strategies for lupus nephritis, briefly review recent advances in under

224 In lupus nephritis, C5-b9 deposits co-localized with IgG, I

225 changes in renal iron homeostasis occurs in lupus nephritis, contributing to the development of kidn

226 CD163 mRNA than did those from patients with lupus nephritis, diabetic nephropathy, or nephrotic synd

227 nt role for FcgammaRs in the pathogenesis of lupus nephritis, suggesting a direct effect on phagocyte

228 t there are different pathogenic pathways in lupus nephritis, the emerging pathogenic mechanism(s) ma

229 ate the distinct functions of Axl and Mer in lupus nephritis, we compared the severity of nephrotoxic

230 we show that BAFF promotes events leading to lupus nephritis.

231 ong been thought to promote inflammation and lupus nephritis.

232 ulonephritis and in a mouse chronic model of lupus nephritis.

233 ficant B cell expansion, BAFF secretion, and lupus nephritis.

234 ajor unmet need for successful management of lupus nephritis.

235 acerbate underlying pathogenic mechanisms in lupus nephritis.

236 l cells associates with viral infections and lupus nephritis.

237 10 wk of age and steadily increases prior to lupus nephritis.

238 ent of immune-mediated nephropathies like in lupus nephritis.

239 in vivo prevented the formation of TLSs and lupus nephritis; however, it did not reduce immune cell

240 Lupus neutrophils produce elevated levels of factors kno

241 and organ damage in the context of neonatal lupus (NL).

242 Severe lupus often includes psychiatric and neurological sequel

243 pDC-associated autoimmune diseases, such as lupus or psoriasis.

244 therapy with belimumab achieved approval for lupus, other BAFF inhibitors were much less beneficial i

245 ontributors beyond B cells are important for lupus pathogenesis.

246 tiple autoimmune diseases, but its effect on lupus pathology remains unclear, with opposing trials in

247 Similarly, RNA sequencing of lupus patient blood revealed similar expression patterns

248 cific changes in gene expression in 8 pooled lupus patient samples treated with interferon (IFN)-beta

249 We performed RNA sequencing of lupus patient whole blood to determine common pathways i

250 autoantibodies mediate pathology in systemic lupus patients and lupus-prone mice.

251 Dead cells accumulated in bone marrow from lupus patients but not from nonautoimmune patients under

252 Keratinocytes from unaffected skin of lupus patients produced significantly more IL-6 compared

253 form is more frequent in CD4(+) T cells from lupus patients than from healthy controls.

254 dependent responses using cells derived from lupus patients, suggesting that inhibition of IRAK4 has

255 gan pathology that affects upwards of 60% of lupus patients.

256 ng of its activity as a potent treatment for lupus patients.

257 rbent assay using human samples of pediatric lupus patients.

258 The most frequent lesions were lupus pernio (n = 21 [46%]) and nodules (n = 20 [43%]).

259 rophils accumulate in SLO over the course of lupus progression, preferentially localizing near T lymp

260 Treatment of lupus-prone B6.Sle1.Yaa mice with an anti-IL-21 blocking

261 DCs in lupus-prone mice we used 7 strains of lupus-prone mice including NZB/W F1, NZB, NZW, NZM2410,

262 t behavioural phenotypes and synapse loss in lupus-prone mice that are prevented by blocking type I i

263 study the function and phenotype of pDCs in lupus-prone mice we used 7 strains of lupus-prone mice i

264 We immunized non-lupus-prone mice with 11 allotype "a" of IgG2a (IgG2a(a)

265 ating leukocyte populations in NZM2328 (NZM) lupus-prone mice with spontaneous chronic glomerulonephr

266 CD8(+) T cells do not cause tissue damage in lupus-prone mice, as genetic ablation of these cells via

267 occurs frequently in patients with lupus and lupus-prone mice, facilitated the development of lethal

268 nd was overexpressed in T1 B cells from BXD2 lupus-prone mice.

269 pression, and polyreactive autoantibodies in lupus-prone mice.

270 and nucleic acid-associated autoimmunity in lupus-prone mice.

271 ate pathology in systemic lupus patients and lupus-prone mice.

272 icrobiota and attenuated SLE-like disease in lupus-prone mice.

273 and engulf neuronal and synaptic material in lupus-prone mice.

274 We used the Sle1 lupus-prone mouse model to examine the role of ICOS in t

275 o understand how MSCs ameliorate symptoms in lupus-prone MRL.Fas(lpr) mice.

276 but not CD11b-deficient mice, and protected lupus-prone MRL/Lpr mice from end-organ injury.

277 Herein, we report that macrophages from lupus-prone MRL/lpr mice have impaired lysosomal maturat

278 and its phenotype and function differ among lupus-prone strains, and these differences may contribut

279 Lupus-related glomerulonephritis was associated with mor

280 ibution of self-memory to the development of lupus-related pathology.

281 CKO mice with a CTSS inhibitor abolished the lupus-related phenotype and reduced the diversity of the

282 Neutrophil depletion early in lupus resulted in a striking acceleration in the onset o

283 with multiple autoimmune diseases, including lupus, scleroderma and Sjogren's syndrome, and had a pro

284 analyzed individually (rheumatoid arthritis; lupus; scleroderma; Sjogren Syndrome; dermatomyositis/po

285 macrophages exhibit a novel transcriptional lupus signature that is conserved within the gene expres

286 Murine and human lupus studies revealed a role for IFN-alpha in vascular

287 vated levels of type I interferon (IFN-I) in lupus, suggesting a direct link between reduced CD11b ac

288 to systemic autoimmunity and that FAAH is a lupus-susceptibility gene that might regulate this proce

289 reactive T cells in mice carrying the Sle1a1 lupus-susceptibility locus.

290 g to peripheral autoimmunity may promote CNS lupus symptoms.

291 hich inhibits oxygen consumption, normalized lupus T cell functions in vitro and reverted disease in

292 Moreover, in cultured human lupus T cells, SHP2 inhibition reduced proliferation and

293 nal center (GC) B cell responses, whereas in lupus they promote aberrant GC responses with autoreacti

294 marinus) tracked for 12 h and a wolf (Canis lupus) tracked for 1 year.

295 CNS lupus typically presents at lupus diagnosis or within th

296 , Comprehensive Clinical Trials Unit at UCL, LUPUS UK, Bayer, National Institute for Health Research

297 Lupus was induced in female wild-type (WT) and P-selecti

298 ution of IL-21 to the pathogenesis of murine lupus, while revealing the importance of T-B cellular cr

299 h microglia transcriptome data, connects CNS lupus with other CNS diseases and provides an explanatio

300 h strongly implicated in the pathogenesis of lupus, with most patients expressing IFN-induced genes i