ライフサイエンスコーパス: interleukin-1alpha

1 n of cyclooxygenase-2 after stimulation with interleukin-1alpha.

2 ion, such as tumor necrosis factor-alpha and interleukin-1alpha.

3 and promote the switch of CAFs to iCAFs via interleukin-1alpha.

4 were subjected to hypoxia and treatment with interleukin-1alpha.

5 imulation with the microenvironmental factor interleukin-1alpha.

6 elial (TBE) cells with a panel of cytokines (interleukin-1alpha, 1beta, 2, 3, 4, 5, 6, 7, 8, 9, 10, 1

7 ed levels of proinflammatory cytokine mRNAs (interleukins 1alpha, 1beta, and 6 and tumor necrosis fac

8 eron-gamma, tumor necrosis factor-alpha, and interleukins 1alpha, 6, 12, 22, 23, and 17.

9 pression of acute proinflammatory cytokines (interleukins 1alpha, 6, and 8, tumor necrosis factor alp

10 and in accumulation of epithelial-associated interleukin-1alpha, a cytokine that inhibits Smad2 signa

11 In addition, interleukin-1alpha, a germ cell-derived cytokine, was al

12 (MABp1) cloned from a human being to target interleukin-1alpha, a mediator of chronic inflammation.

13 The responses to interleukin-1alpha, a photoinduced cytokine, were marked

14 ar clearance and tear fluid concentration of interleukin-1alpha, a proinflammatory cytokine that has

15 sis, in part through a process that requires interleukin-1alpha activation.

16 Neutralization of interleukin-1alpha activity suppressed the constitutive

17 Interleukin-1alpha, although activated in VZV-infected c

18 did poorly metastatic clones in response to interleukin 1alpha and IFN-gamma stimulation.

19 terized by an elevated CCL2 level, decreased interleukin 1alpha and interleukin 1beta cervical concen

20 gnificantly lower levels of 2 key cytokines--interleukin 1alpha and interleukin 8--at wound sites.

21 tein was shown to stimulate the secretion of interleukin 1alpha and RANTES, whereas purified F (fusio

22 uman saphenous vein SMCs stimulated with IL (interleukin)-1alpha and PDGF (platelet-derived growth fa

23 Cytokines interleukin-1alpha and -1beta, tumor necrosis factor-alp

24 amycin-treated mice reduced plasma levels of interleukin-1alpha and -beta and granulocyte-colony stim

25 vely, by basic fibroblast growth factor plus interleukin-1alpha and antisense oligonucleotides to PKC

26 r necrosis, and resulted in up-regulation of interleukin-1alpha and down-regulation of anti-apoptotic

27 The efficacy and safety of rilonacept, an interleukin-1alpha and interleukin-1beta cytokine trap,

28 acrophages alongside inflammasome-associated interleukin-1alpha and interleukin-1beta production prom

29 Interleukin-1alpha and interleukin-1beta were first incr

30 For example, both interleukin-1alpha and interleukin-33 exhibit 'alarmin'-

31 Moreover, interleukin-1alpha and interleukin-6 did not impair the

32 ocused on the role of bacterial lipases, and interleukin-1alpha and matrix metalloproteinases in the

33 ooth muscle cells following stimulation with interleukin-1alpha and platelet-derived growth factor.

34 man corneal fibroblasts after treatment with interleukin-1alpha and subjected to DNA microarray analy

35 production of the pro-inflammatory cytokines interleukin-1alpha and tumor necrosis factor alpha in th

36 as accompanied by decreased plasma levels of interleukin-1alpha and tumor necrosis factor alpha, and

37 Interleukin-1alpha and tumor necrosis factor-alpha enhan

38 (KC), macrophage cationic peptide-1 (MCP-1), interleukin 1alpha, and interleukin 6) involved in monoc

39 macrophage inflammatory proteins 1 and 2 and interleukin-1alpha, and higher levels of putative protec

40 igand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with

41 or necrosis factor-alpha, interleukin-15 and interleukin-1alpha, and transforming growth factor-beta.

42 espectively) and was effective in inhibiting interleukin-1alpha- and oncostatin M-induced C1,C2 relea

43 Further study of MABp1 anti-interleukin-1alpha antibody therapy for advanced stage c

44 As tumor necrosis factor-alpha and interleukin-1alpha are major mediators of cutaneous infl

45 mokines and we report the failure to release interleukin-1alpha as a common immunological phenotype.

46 ased expression of c-myc (5- to 12-fold) and interleukin-1alpha/beta (600-fold) by real-time polymera

47 tumor necrosis factor-alpha (TNF-alpha) and interleukin-1alpha/beta (IL-1alpha/beta) that contribute

48 ess the safety and tolerability of MABp1 for interleukin-1alpha blockade in a refractory cancer popul

49 on exogenous microglia induced expression of interleukin-1alpha by the organotypic culture.

50 ical immunosensor for sensitive detection of interleukin 1alpha cancer biomarker was described by usi

51 The interleukin-1alpha concentration remained increased unti

52 uropathogenic GBS-specific up-regulation of interleukin 1alpha during infection.

53 ry cytokines tumor necrosis factor-alpha and interleukin-1alpha elevate RANKL and OPG expression 5-40

54 ctive MMP activity on the aggrecan IGD; (ii) interleukin-1alpha exposure induces both aggrecanase and

55 Our results demonstrate that regulation of interleukin-1alpha expression is primarily dependent on

56 d growth factor-BB, insulin growth factor-1, interleukin-1alpha) failed to augment the adhesion or pr

57 Interleukin-1alpha had a repulsive chemotactic effect on

58 MABp1, an antibody that targets interleukin 1alpha, has been associated with antitumour

59 e nuclear localisation sequence in their pro-interleukin-1alpha, histone acetyltransferase binding ab

60 une correlative studies showed a decrease in interleukin -1alpha (IL-1alpha), IL-21, and tumor necros

61 expression of the bone resorptive cytokines interleukin 1alpha (IL-1alpha) (P < 0.01) and IL-1beta (

62 nduced steady increases in the expression of interleukin 1alpha (IL-1alpha) and IL-18.

63 Interleukin 1alpha (IL-1alpha) and IL-1beta are equally

64 ractant CCL20, and proinflammatory cytokines interleukin 1alpha (IL-1alpha) and IL-1beta.

65 results indicated the presence of mRNAs for interleukin 1alpha (IL-1alpha) and transforming growth f

66 in multiple cell types after treatment with interleukin 1alpha (IL-1alpha) as compared with tumor ne

67 ot have a marked effect on the expression of interleukin 1alpha (IL-1alpha) during infection.

68 Interleukin 1alpha (IL-1alpha) is capable of driving pro

69 g26 CD4(+) T cells consistently exhibit high interleukin 1alpha (IL-1alpha) levels with no significan

70 Mechanistically, deficiency in interleukin 1alpha (IL-1alpha) or platelet-activating fa

71 o immunomodulatory therapeutics.The cytokine interleukin 1alpha (IL-1alpha) plays an important role i

72 g greater lung damage, vascular leakage, and interleukin 1alpha (IL-1alpha) release than the low-viru

73 Interleukin 1alpha (IL-1alpha), a 33 kDa precursor, is c

74 in response to tumor necrosis factor alpha, interleukin 1alpha (IL-1alpha), gamma interferon, lipopo

75 ection 3 d later as well as their content of interleukin 1alpha (IL-1alpha), IL-1beta, and IL-6.

76 ctor (GM-CSF), gamma interferon (IFN-gamma), interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, and IL-1

77 d secretion of the proinflammatory cytokines interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, IL-12p70

78 led significant differences in expression of interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, IL-1Ra,

79 weight (LW/BW) ratio, and elevated levels of interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, tumor ne

80 sets of monocytes by assessing intracellular interleukin 1alpha (IL-1alpha), IL-1beta, interleukin 6

81 No upregulation of antral mucosal interleukin 1alpha (IL-1alpha), IL-1beta, or tumor necro

82 anulocyte colony-stimulating factor (G-CSF), interleukin 1alpha (IL-1alpha), IL-6, IL-9, RANTES, tumo

83 ally pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h.

84 s (EC) to tumor necrosis factor-alpha (TNF), interleukin-1alpha (IL-1), and phorbol myristate acetate

85 posed to phorbol ester (TPA) or PDGF-BB plus interleukin-1alpha (IL-1).

86 /- 2.08 pg/ml in healthy people, p < 0,001), interleukin-1alpha (IL-1alpha) - by 5.08 times (51.55 +/

87 Cytokines that were upregulated included interleukin-1alpha (IL-1alpha) and -1beta, IL-1 receptor

88 eolar macrophages (AMs), which then released interleukin-1alpha (IL-1alpha) and caused inducible bron

89 temic levels of the proinflammatory cytokine interleukin-1alpha (IL-1alpha) and higher levels of the

90 While levels of interleukin-1alpha (IL-1alpha) and IL-16 were among 10 p

91 Neutrophils unable to produce interleukin-1alpha (IL-1alpha) and IL-1beta (IL-1alpha/b

92 Interleukin-1alpha (IL-1alpha) and IL-1beta are potent i

93 Here, we report that interleukin-1alpha (IL-1alpha) and IL-1beta are released

94 Neutralizing antibodies against interleukin-1alpha (IL-1alpha) and IL-1beta completely b

95 in increased circulating cytokines, such as interleukin-1alpha (IL-1alpha) and IL-1beta, and increas

96 nensis-infected DCs secreted lower levels of interleukin-1alpha (IL-1alpha) and IL-1beta, were less p

97 expression of the proinflammatory cytokines interleukin-1alpha (IL-1alpha) and IL-1beta.

98 ificant induction of mRNAs for the cytokines interleukin-1alpha (IL-1alpha) and IL-6 and the chemokin

99 colony-stimulating factor, interferon-gamma, interleukin-1alpha (IL-1alpha) and IL-6, compared with m

100 ious levels constitutively with considerable interleukin-1alpha (IL-1alpha) and tumor necrosis factor

101 icular cartilage explants were cultured with interleukin-1alpha (IL-1alpha) and/or oncostatin M (OSM)

102 Blocking experiments with neutralizing anti-interleukin-1alpha (Il-1alpha) antibodies and IL-1Ra, an

103 Expression of the genes for collagenase and interleukin-1alpha (IL-1alpha) are induced as stromal ce

104 dent upon the release of the nuclear alarmin interleukin-1alpha (IL-1alpha) by dying cells.

105 and tested for the presence of TNFalpha and interleukin-1alpha (IL-1alpha) by enzyme-linked immunoso

106 This study was performed to determine if interleukin-1alpha (IL-1alpha) combined with other proin

107 Intratracheal LPS induced release of pro-interleukin-1alpha (IL-1alpha) from necrotic alveolar ma

108 Caspase-11 and GSDMD mediate the release of interleukin-1alpha (IL-1alpha) in allo-HSCT.

109 Aggrecan catabolism was induced by interleukin-1alpha (IL-1alpha) in normal human articular

110 ficiency enhances the early local release of interleukin-1alpha (IL-1alpha) in response to damaged ce

111 Recently, we demonstrated a role for interleukin-1alpha (IL-1alpha) in the establishment of i

112 Interleukin-1alpha (IL-1alpha) is a key danger signal re

113 Interleukin-1alpha (IL-1alpha) is a multifunctional cyto

114 Interleukin-1alpha (IL-1alpha) is a potent proinflammato

115 Interleukin-1alpha (IL-1alpha) is a powerful activator o

116 nal protein production in response to either interleukin-1alpha (IL-1alpha) or lipopolysaccharide (LP

117 % O(2) (normoxia) in media supplemented with interleukin-1alpha (IL-1alpha) or tumor necrosis factor

118 ingest apoptotic eosinophils was enhanced by interleukin-1alpha (IL-1alpha) or tumor necrosis factor

119 emonstrate that the proinflammatory cytokine interleukin-1alpha (IL-1alpha) plays an essential role i

120 d bone marrow-derived neutrophils exposed to interleukin-1alpha (IL-1alpha) produced chemokines in an

121 Enhanced interleukin-1alpha (IL-1alpha) production from ER-stress

122 Here, we demonstrated that interleukin-1alpha (IL-1alpha) signaling through IL-1R a

123 role in BTB restructuring via the action of interleukin-1alpha (IL-1alpha) since germ cells are know

124 elease from megakaryocytes can be induced by interleukin-1alpha (IL-1alpha) via a new rupture mechani

125 We previously demonstrated that interleukin-1alpha (IL-1alpha) was critical for the indu

126 f the TNF-induced transcripts analyzed, only interleukin-1alpha (IL-1alpha) was modulated in response

127 treating (a) bovine articular cartilage with interleukin-1alpha (IL-1alpha), (b) purified bovine COMP

128 Here we report that the cytokine interleukin-1alpha (IL-1alpha), an alarmin, is necessary

129 Interestingly, interleukin-1alpha (IL-1alpha), an important pro-inflamm

130 ransforming growth factor-alpha (TGF-alpha), interleukin-1alpha (IL-1alpha), and IL-1 receptor antago

131 f proinflammatory cytokines, such as GRO/KC, interleukin-1alpha (IL-1alpha), and IL-1beta.

132 ed to thrombopoietin (TPO), kit ligand (KL), interleukin-1alpha (IL-1alpha), and IL-3 in serum-free c

133 of tumor necrosis factor alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), and IL-6 in DCs, althoug

134 r chondrocytes were cultured with or without interleukin-1alpha (IL-1alpha), and the relative express

135 Mouse platelets expressed interleukin-1alpha (IL-1alpha), but not IL-1beta, induce

136 rophages with Legionella pneumophila induced interleukin-1alpha (IL-1alpha), IL-10, monocyte chemotac

137 d against interferon-alpha, interferon-beta, interleukin-1alpha (IL-1alpha), IL-12p35, IL-12p40, and

138 ony-stimulating factor (G-CSF) and decreased interleukin-1alpha (IL-1alpha), IL-1beta, and IL-4 in CB

139 creased expression of mRNA for the cytokines interleukin-1alpha (IL-1alpha), IL-1beta, and IL-8 but n

140 nes tumor necrosis factor alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), IL-1beta, and IL-8 were

141 Fibroblasts from relb(-/-) mice overexpress interleukin-1alpha (IL-1alpha), IL-1beta, and tumor necr

142 Interleukin-1alpha (IL-1alpha), IL-1beta, IL-2, IL-4, IL

143 is reflected at the translational level, as interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, and tumo

144 ing antisense RNA probes specific for bovine interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, gamma in

145 gene c-myc and the proinflammatory cytokines interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IFN-gamm

146 ater proportion of RA cases versus controls: interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IL-10, I

147 ificant up-regulation in gene expression for interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IL-10, t

148 ansgenic mice showed identical expression of interleukin-1alpha (IL-1alpha), IL-1beta, interferon gam

149 ed, immature DCs exhibited higher amounts of interleukin-1alpha (IL-1alpha), IL-1beta, tumor necrosis

150 is, we examined expression of genes encoding interleukin-1alpha (IL-1alpha), IL-2, IL-4, IL-5, IL-6,

151 for tumor necrosis factor alpha (TNF alpha), interleukin-1alpha (IL-1alpha), IL-4, IL-6, IL-8, macrop

152 hallenged with IOE had lower levels of serum interleukin-1alpha (IL-1alpha), IL-6, and IL-10 compared

153 ators of the acute-phase response, including interleukin-1alpha (IL-1alpha), IL-6, and tumor necrosis

154 pared to the attenuated mutant were noted in interleukin-1alpha (IL-1alpha), IL-6, IL-8, and tumor ne

155 Up-regulated genes included interleukin-1alpha (IL-1alpha), IL-8, and thrombomodulin

156 bFGF, interleukin-1alpha (IL-1alpha), IL-8, and tumor necrosis

157 ized expression of proinflammatory cytokines interleukin-1alpha (IL-1alpha), macrophage inflammatory

158 actor receptor-associated protein 1 (TRAF1), interleukin-1alpha (IL-1alpha), MCP-2, N-cadherin, and b

159 to be highly synergistic in the induction of interleukin-1alpha (IL-1alpha), type II (inducible) nitr

160 tion-polymerase chain reaction (RT-PCR) with interleukin-1alpha (IL-1alpha)-specific primers using to

161 Interleukin-1alpha (IL-1alpha)-stimulated stromelysin pr

162 were cultured with 1 microM RetA or in 3 nM interleukin-1alpha (IL-1alpha).

163 tro produced tumor necrosis factor alpha and interleukin-1alpha (IL-1alpha).

164 lines constitutively produce high levels of interleukin-1alpha (IL-1alpha).

165 the surrounding tissue through the cytokine interleukin-1alpha (IL-1alpha).

166 inomycin D, and the proinflammatory cytokine interleukin-1alpha (IL-1alpha).

167 itamin D(3) was the proinflammatory cytokine interleukin-1alpha (IL-1alpha).

168 It is also possible to measure release of interleukin-1alpha (IL-1alpha).

169 rtilage chondrocytes treated with or without interleukin-1alpha (IL-1alpha).

170 diated through the proinflammatory cytokine, interleukin-1alpha (IL-1alpha).

171 as stimulated to resorb with the addition of interleukin-1alpha (IL-1alpha)/oncostatin M (OSM) in the

172 Interleukin-1alpha (IL-1alpha)is a prototypical proinfla

173 ced by direct injection of recombinant human interleukin-1alpha (IL-1alpha, 1 microg in 2 microL) int

174 Histamine (100 microM) and interleukin-1alpha (IL-1alpha, 10 ng/ml) significantly s

175 various stimuli, including cytokines (e.g., interleukin-1alpha [IL-1alpha] and tumor necrosis factor

176 nce and absence of added exogenous cytokine (interleukin-1alpha [IL-1alpha] or tumor necrosis factor

177 oattractant protein 1]) and three cytokines (interleukin-1alpha [IL-1alpha], IL-10, and granulocyte c

178 were analyzed for cytokine production (i.e., interleukin-1alpha [IL-1alpha], IL-1beta, IL-6, IL-8, IL

179 e markers within 8 candidate cytokine genes (interleukin-1alpha [IL-1alpha], IL-2, IL-4, IL-6, IL-10,

180 x (MAC) bacteremia, the levels of IL-1alpha (interleukin-1alpha), IL-6, IL-10, tumor necrosis factor

181 nd plasma inflammatory cytokines (IL-1alpha [interleukin 1alpha], IL-17A [interleukin 17A], P<0.05) i

182 Interleukin-1alpha (IL1A) is both regulated by and able

183 [CKB], angiotensin-converting enzyme [DCP1], interleukin-1alpha [IL1A], low-density lipoprotein recep

184 is initiated by the paracrine signalling of interleukin 1alpha (IL1alpha), which activates both skin

185 inducible form of nitric-oxide synthase and interleukin-1alpha in RAW 264.7 cells.

186 cted mice produced tumor necrosis factor and interleukin-1alpha in response to T4SS-sufficient, but n

187 king synergy between ultraviolet B and added interleukin-1alpha in the induction of transcription by

188 ighly conserved regions in the pro-domain of interleukin-1alpha, including a nuclear localisation seq

189 or significantly decreased recombinant human interleukin-1alpha-induced hypercalcemia.

190 tumor necrosis factor-alpha (TNF-alpha)- and interleukin-1alpha-induced NF-kappaB activity and an enh

191 in synergy with lipopolysaccharide (LPS) or interleukin 1alpha induces Cox-2 expression in mouse per

192 ormants was stimulated by several cytokines (interleukin 1alpha, interleukin 6, and tumor necrosis fa

193 o induce inflammation-related genes, such as interleukin-1alpha, interleukin-1beta, interleukin-6, an

194 Interleukin-1alpha, interleukin-1beta, or live Pseudomon

195 in the expression of inflammatory cytokines (interleukin-1alpha, interleukin-1beta, or tumor necrosis

196 reversed increases in inflammatory mediators interleukin-1alpha, interleukin-1beta, tissue necrosis f

197 10) and higher levels of interleukin-1beta, interleukin-1alpha, interleukin-6, interleukin-8, interl

198 r cells was induced by a single injection of interleukin-1alpha into the lacrimal gland and that this

199 Interleukin-1alpha is a suggested dual-function cytokine

200 Human interleukin-1alpha is transported across the murine bloo

201 d by serum interferon-induced protein 10 and interleukin 1alpha, is independently associated with inc

202 tumor necrosis factor alpha levels and serum interleukin-1alpha levels compared with animals with art

203 decrease in tumor necrosis factor-alpha and interleukin-1alpha levels in the oxazalone-treated epide

204 xide synthase, the proinflammatory cytokines interleukin-1alpha, macrophage inflammatory protein 1-al

205 (PKC) in basic fibroblast growth factor- and interleukin-1alpha-mediated MMP production from cultured

206 tatic cancer (18 tumour types) received anti-interleukin-1alpha monotherapy in dose-escalation and ex

207 ophages in the dermis and a reduced level of interleukin-1alpha mRNA expression, compared with WT mic

208 With the exception of interleukin-1alpha, none of the humoral factors changed

209 d validate inactivating mutations in the pro-interleukin-1alpha nuclear localisation sequence of mult

210 onserved in those species that have lost pro-interleukin-1alpha nuclear localisation.

211 or 2 and interleukin 17F, without effects on interleukin 1alpha or interleukin 1beta, suggesting a di

212 Treatment with interleukin-1alpha or interleukin-6 of cultured composit

213 ted protein kinase by tumor necrosis factor, interleukin-1alpha, or gamma-interferon.

214 Tumor necrosis factor-alpha (TNF-alpha), interleukin-1alpha, or interleukin-1beta caused a time-d

215 levels of CXCL10 (C-X-C motif chemokine 10), interleukin-1alpha, placental growth factor, and platele

216 genes proximal to SMILR was also altered by interleukin-1alpha/platelet-derived growth factor treatm

217 Interleukin-1alpha plus ultraviolet B caused a remarkabl

218 Only interleukin-1alpha possibly fulfills the criteria which

219 inding domain which resembles the NLS of the interleukin-1alpha precursor.

220 alysis of the corneal fibroblast response to interleukin-1alpha provides important insight into model

221 S to uroepithelium and vigorous induction of interleukin 1alpha represents the initial stages of GBS

222 untreated or treated with recombinant human interleukin-1alpha (rHuIL-1alpha), was assessed by radio

223 In contrast, addition of rIL (interleukin)-1alpha, rIL-1beta, rIL-6, or rIL-12 did not

224 and protein interactome, and how this shaped interleukin-1alpha's intracellular role, is unknown.

225 Why evolution modified pro-interleukin-1alpha's subcellular location and protein in

226 in an increase in tumor necrosis factor and interleukin-1alpha staining in the epidermis that was re

227 derived cytokines tumour necrosis factor and interleukin-1alpha stimulated reactive oxygen species an

228 In interleukin-1alpha-stimulated epidermal cultures, human

229 onoclonal antibody binding for E-selectin in interleukin-1alpha-stimulated microvascular endothelium

230 We thus compared the effects of interleukin-1alpha stimulation and neuronal induction of

231 Within five hours of interleukin-1alpha stimulation, E-selectin density incre

232 ry cytokines tumor necrosis factor alpha and interleukin 1alpha, strongly potentiated IFN-gamma-induc

233 ow that TurboID proximity labelling with pro-interleukin-1alpha suggests a nuclear role for pro-inter

234 eukin-1alpha suggests a nuclear role for pro-interleukin-1alpha that involves interaction with histon

235 Without added interleukin-1alpha the two constructs produced similar b

236 ated by transforming growth factor-alpha and interleukin-1alpha, the model revealed new molecular mec

237 This and the failure of recombinant interleukin-1alpha to stimulate peripheral blood mononuc

238 h polymyositis and dermatomyositis implicate interleukin-1alpha, transforming growth factor-beta, and

239 The tumor produced transcripts for interleukin-1alpha, tumor necrosis factor-alpha, and int

240 ctor-alpha (TGF-alpha), but not by cytokines interleukin-1alpha, tumor necrosis factor-alpha, interfe

241 increase in DNA binding, but treatment with interleukin-1alpha, tumor necrosis factor-alpha, or phor

242 about how proinflammatory cytokines, such as interleukin-1alpha/tumor necrosis factor-alpha/C1q (ITC)

243 Further investigation showed that interleukin-1alpha was the primary cytokine secreted by

244 els of serum tumor necrosis factor alpha and interleukin 1alpha were detected.

245 Interleukin-1alpha, when normalized to baseline, increas

246 pa B-dependent transcriptional regulation of interleukin-1alpha, which, in an autocrine manner, induc

247 toinduced cytokine, were markedly different: interleukin-1alpha without ultraviolet produced a 15-fol