ライフサイエンスコーパス: IL-16

1 IL-16 actions were found to be mediated by the autocrine

2 IL-16 also elicited brefeldin A-inhibitable, vesicular t

3 IL-16 and RANTES protein levels, as determined by specif

4 IL-16 binds to CD4 and induces a migratory response in C

5 IL-16 delivery vectors could be exploited to prevent or

6 IL-16 dose dependently (0.01-100 nM) elicited new lipid

7 IL-16 expression and the mechanism involved in its regul

8 IL-16 has been characterized only in the immune system,

9 IL-16 induced the rapid vesicular transport-mediated rel

10 IL-16 is a CD4(+)-specific chemoattractant and RANTES is

11 IL-16 is a novel cytokine, which is chemoattractant for

12 IL-16 is a proinflammatory cytokine implicated in the pa

13 IL-16 is a proinflammatory cytokine that signals via CD4

14 IL-16 is synthesized as a precursor molecule of 68 kDa (

15 IL-16 messenger RNA and protein levels in inflammatory b

16 IL-16 protein and activity are undetectable in fibroblas

17 IL-16 structure and function are highly conserved across

18 IL-16, a ligand for CD4, is a chemoattractant molecule e

19 IL-16-mediated ligation of CD4 expressed on CD8 T cells

20 IL-16/CD4 inhibition of SDF-1alpha/CXCR4 signals require

21 IL-16/CD4 stimulation does not result in surface modulat

22 IL-16/IL-2 cotreatment did not appear to induce selectiv

23 Interleukin-1beta (IL-1beta), IL-10, IL-16, IL-17, RANKL, tumor necrosis factor alpha (TNFalp

24 -2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p35, IL-16, and IL-18, as well as genes encoding gamma interf

25 IL-7, IL-8, IL-12/IL-23p40, IL-12p70, IL-13, IL-16, IP-10, MCP-1, MCP-4, MDC, MIP-1a, TARC, TNFB) was

26 eron-gamma, interleukin [IL]-6, IL-8, IL-15, IL-16, IL-17, CXCL10 [IP-10], and MCP-1 [CCL2]) in BAL s

27 terleukin 1 (IL-1), IL-2, IL-6, IL-8, IL-15, IL-16, IL-17, IL-18, or gamma interferon (IFN-gamma) gen

28 n exogenous CD8+ T cells deficient in IL-16 (IL-16(-/-)) were infused into CD8(-/-) mice immediately

29 3 activity of hepatocellular interleukin 16 (IL-16) is no longer processed and released.

30 ated CD8 cells to respond to interleukin 16 (IL-16), a ligand that binds CD4 and induces cellular che

31 Interleukin-16 (IL-16) activates CD4(+) cells, possibly by direct intera

32 Interleukin-16 (IL-16) is a pleiotropic cytokine that functions as a che

33 Interleukin-16 (IL-16) is reported to be a chemoattractant cytokine and

34 he immunomodulatory cytokine interleukin-16 (IL-16) represents the secreted C-terminus of a larger pr

35 rivascular space and secrete interleukin-16 (IL-16), a potent chemoattractant for monocytes and CD4+

36 P-9, OPN, PF4, SDF-1) and cytokines (IL-1ra, IL-16) in BM Soup.

37 cells, and, in long-term cultures with IL-2, IL-16 facilitates the expansion of CD4(+)CD25(+) cells.

38 vement of alarmins such as IL-1alpha, IL-33, IL-16, and high-mobility group box 1 in cellular and phy

39 several inflammatory cytokines (IL-6, IL-7, IL-16, and IL-17) and increased necrosis in older cells.

40 55 [95% confidence interval {CI}, .37-.78]), IL-16/tumor necrosis factor-alpha (OR, 0.66 [95% CI, .45

41 ate that PBEF stimulated expression of IL-8, IL-16, and CCR3 via its non-enzymatic activity.

42 y cytokines, including IL-1beta, IL-6, IL-8, IL-16, and tumor necrosis factor-alpha accompanying the

43 on levels of eotaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta were significantly high

44 wever, little information is available about IL-16 function in human pregnancy.

45 by this enzyme releases biologically active IL-16 from its inactive precursor.

46 In addition, IL-16 has an immunomodulatory role in asthmatic inflamma

47 ages, and it could be blocked by Abs against IL-16, a CD8+ T cell-derived cytokine.

48 ule-1 (CD31), P-selectin (CD62), IL-1 alpha, IL-16, and granulocyte chemoattractant protein-2 were do

49 owever, CD3/CD28 costimulation did not alter IL-16 mRNA appearance or stability in either CD4+ or CD8

50 It is postulated that CD4 is an IL-16 receptor, although other receptors or coreceptors

51 [IP-10]: 107.0 vs. 31.9 pg/mL [P=0.001] and IL-16: 472.1 vs. 283.01 pg/mL [P=0.01]).

52 The levels of both CXCL10 (IP-10) and IL-16 were significantly increased in histologically pro

53 interferon alpha, interleukin 1 [IL-1], and IL-16); and chemokines (macrophage inflammatory protein-

54 Detection of high levels of IL-1alpha and IL-16 in plasma and the independence of these protein le

55 levels of interleukin-1alpha (IL-1alpha) and IL-16 were among 10 proteins found to be significantly e

56 cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significantly increased in MPs from acute CF

57 In contrast, the genes encoding TGF-beta and IL-16 were expressed at lower levels in lymph nodes from

58 between energy metabolism, eosinophils, and IL-16 content are not direct or straightforward.

59 central role of T-bet, Tim-3, IFN-gamma, and IL-16 in mediating this pathogenic tissue response.

60 Covalent linkage of the NAg and IL-16 was required for inhibition of experimental autoim

61 riostin), TH9/IL-9, IL-23 (p40 and p19), and IL-16 mediators (all P < .05).

62 Anti-IL-16 mAb reduced colonic injury and inflammation induce

63 Anti-IL-16 mAb treatment significantly reduced TNBS-induced w

64 tially susceptible to neutralization by anti-IL-16 and anti-RANTES Abs.

65 The 14.1 antibody is a monoclonal anti-IL-16 antibody, which when incubated with CD4(+) cells i

66 reated with vehicle, TNBS alone, TNBS + anti-IL-16 monoclonal antibody (mAb), TNBS + control mAb, or

67 an express IL-16 mRNA and protein as well as IL-16-dependent chemoattractant activity.

68 rofound variability of eosinophil-associated IL-16 (CV = 103%).

69 4 Fab, soluble CD4, and a CD4 domain 4-based IL-16 blocking peptide inhibited the actions of IL-16 on

70 ter), nor was there any relationship between IL-16 content and the characterized -295T/C IL-16 promot

71 Although bioactive IL-16 protein is present in unstimulated CD8+ T cells, t

72 imulated CD8+ T cells, there is no bioactive IL-16 present in CD4+ T cells.

73 The secretion of bioactive IL-16 from CD4+ T cells correlated with the appearance o

74 chanism of release or secretion of bioactive IL-16 is currently unknown, but does not correlate with

75 Peptides A and B also blocked IL-16 binding to CD4 in vitro, whereas peptide C did not

76 on peptides (designated A, B, and C) blocked IL-16 chemoattractant activity, with peptide B the most

77 5-Lipoxygenase inhibitors blocked IL-16-, eotaxin-, and RANTES-induced IL-4 release; but n

78 the lung in a dendritic cell-independent but IL-16-dependent process and diminish neutrophil recruitm

79 Desensitization of CCR5 by IL-16 required at least 10 min of pretreatment; no modul

80 Desensitization of CXCR4 by IL-16 required at least 10-15 min pretreatment; no modul

81 IL-16 content and the characterized -295T/C IL-16 promoter polymorphism.

82 in serum (e.g. E-selectin, PI3/elafin, CCL7, IL-16) correlated with SCORAD, but not BMI.

83 As a natural ligand for CD4, IL-16 has been shown to preferentially induce migration

84 ization induced by a natural ligand for CD4, IL-16, is distinct from the inhibitory effects induced b

85 ith Abs to the Th1-selective chemoattractant IL-16 show significantly less adhesion formation than wi

86 e CD4-specific T lymphocyte chemoattractant, IL-16, and RANTES, a C-C chemokine, in their fibroblasts

87 e expression of the T cell chemoattractants, IL-16 and RANTES.

88 tients, express the T cell chemoattractants, IL-16, and RANTES.

89 related activation-induced cytokine, CHI3L1, IL-16, and matrix metalloproteinase-12 were cardiovascul

90 Colonic IL-16 protein levels were increased in patients with Cro

91 We have previously reported constitutive IL-16 mRNA expression and pro-IL-16 protein in CD4+ and

92 our data demonstrate that monocytes contain IL-16 that is released during spontaneous apoptosis.

93 By contrast, IL-16/CD4 desensitization of MIP-1ss/CCR5 responses requ

94 Cytokine IL-16 plays an important role in innate immune responses

95 ression of two other inflammatory cytokines: IL-16 and CCR3.

96 ppression by attenuating caspase-3-dependent IL-16 processing and release, which concomitantly preven

97 Furthermore, elevated IL-16 levels are found in the sera from patients with AI

98 attle, while expression of the gene encoding IL-16 was lower in tissues from infected cattle than in

99 etween any of these cytokines and eosinophil IL-16 content.

100 und no direct correlation between eosinophil IL-16 content and donor age, sex, total leukocytes, lymp

101 sulted in a 2.7-fold reduction in eosinophil IL-16 content among C57BL/6-IL5tg mice.

102 Interestingly, eosinophil IL-16 content correlated directly with body mass index (

103 fibroblasts from several tissues can express IL-16 mRNA and protein as well as IL-16-dependent chemoa

104 at fibroblasts from patients with GD express IL-16, a CD4-specific chemoattractant, and RANTES, a C-C

105 omed to the ischemic hind limb and expressed IL-16.

106 Whether the constitutively expressed IL-16 acts intracellularly, extracellularly, or both is

107 inant of the H129 strain of HSV-1 expressing IL-16, a cytokine with lymphocytic and monocytic chemoat

108 Cells expressing IL-16 linked to a signal peptide secrete considerably mo

109 tends to almost 25 days for cells expressing IL-16 with signal peptide as compared with only 15 days

110 6 into the supernatant than cells expressing IL-16 without a signal peptide and are considerably more

111 g toward the CD4-specific chemotactic factor IL-16, providing another function for the CD4 molecule o

112 The precursor for IL-16 (pro-IL-16) is a nuclear and cytoplasmic PDZ domai

113 e solution structure previously reported for IL-16 reveals a tryptophan residue obscuring the recogni

114 The D4 residues required for IL-16 binding overlap those previously shown to particip

115 56lck enzymatic activity is not required for IL-16-induced migration, it was required for desensitiza

116 ed in Crohn's disease, suggesting a role for IL-16 in the pathophysiology of inflammatory bowel disea

117 omplex class II, contains a binding site for IL-16 in the D4 domain.

118 It appears that the sole target for IL-16 is the CD4-bearing cell.

119 d C-terminal IL-16 sequences were tested for IL-16 inhibition.

120 y released from fibroblasts not derived from IL-16 can be attributed to RANTES.

121 Among several known functions, IL-16 is a chemoattractant factor for CD4+ T cells and i

122 culation of BALB/c mice with H129wt and H129/IL-16 resulted in a delay of virus spread to the hypotha

123 d eyes of mice infected with H129wt and H129/IL-16 than in mice infected with H129wt and/or H129wt an

124 lated in the AC with H129wt, H129wt and H129/IL-16, or H129wt and H129/pGal10 (a recombinant virus co

125 f mice infected with H129wt, H129wt and H129/IL-16, or H129wt and H129/pGal10 was similar, more Mac-1

126 creased IL-16 binding vs CD4 alone; however, IL-16 could not bind to CCR5 alone.

127 ity comparing the predicted murine and human IL-16 precursor proteins (pro-IL-16).

128 nsfected with the C-terminal 130 aa of human IL-16 are rendered resistant to HIV infection.

129 nding to the 16 C-terminal residues of human IL-16 inhibits chemoattractant activity.

130 Therapy for 14 days with recombinant human IL-16 significantly inhibited the production of IFN-gamm

131 These data identify IL-16 as an optimal cytokine partner for the generation

132 When exogenous CD8+ T cells deficient in IL-16 (IL-16(-/-)) were infused into CD8(-/-) mice immed

133 at both N-terminal and C-terminal domains in IL-16 participate in receptor binding or activation.

134 nase-associated protein 2 mRNA expression in IL-16 null mice, but basal expression and activation-dep

135 ansiently greater thymidine incorporation in IL-16-deficient CD4(+) T cells than wild-type controls,

136 Point mutations in IL-16 revealed that Arg107 is critical for chemoattracta

137 We also measured significantly increased IL-16 and stem cell factor in KC saliva samples compared

138 The presence of CCR5 significantly increased IL-16 binding vs CD4 alone; however, IL-16 could not bin

139 01), respectively, indicating that increased IL-16 levels in PE is associated with the severity of th

140 GD-IgG can also induce IL-16 in RA fibroblasts, and RA-IgG shows similar activi

141 Furthermore, RA-IgG fails to induce IL-16 or RANTES expression in synovial fibroblasts from

142 data indicate that at sites of inflammation IL-16 may contribute to selective Treg cell expansion th

143 G-protein coupled, pertussis toxin inhibited IL-16-induced eosinophil activation.

144 , -2, or -3 stimulation, completely inhibits IL-16/CD4-induced T cell migration.

145 was paralleled by the loss of intracellular IL-16, as detected by flow cytometry, and the concurrent

146 erproliferative phenotype in T cells lacking IL-16.

147 atment of T cells with a natural CD4 ligand, IL-16, could alter cellular responsiveness to macrophage

148 concentrations of CD40 antigen, CD40 ligand, IL-16, monocyte chemotactic protein-1, and vascular cell

149 r signaling through CD4 by a natural ligand, IL-16, could alter cellular responsiveness to chemokine

150 ion, but did not change inflammatory markers IL-16 and eosinophil peroxidase.

151 -terminal peptide of 121 amino acids (mature IL-16), which is cleaved from the precursor protein (pro

152 , one of which is present in secreted mature IL-16.

153 o a signal peptide secrete considerably more IL-16 into the supernatant than cells expressing IL-16 w

154 Colonic mucosal IL-16 levels were elevated in Crohn's disease, suggestin

155 nctional similarity between human and murine IL-16 and suggest that amino acids in the C terminus are

156 To that end, we cloned the murine IL-16 cDNA and found a high degree of amino acid similar

157 ion and characterization of a large neuronal IL-16 precursor, NIL-16.

158 ulatory role, we investigated the ability of IL-16 to recruit and influence the development of T regu

159 16 blocking peptide inhibited the actions of IL-16 on eosinophils.

160 The anti-inflammatory activity of IL-16 in rheumatoid synovitis was confirmed by treating

161 emoattractant and MLR-inhibitory activity of IL-16.

162 The amount of IL-16 protein released into the medium is 3- to 4-fold g

163 ies new opportunities for the development of IL-16-targeted therapeutics, including small molecules t

164 ut the processing and tissue distribution of IL-16 and pro-IL-16, we investigated the distribution of

165 o-IL-16, we investigated the distribution of IL-16 mRNA and protein in human lymphoid tissue.

166 kine receptors, we determined the effects of IL-16 interaction with CD4 on CXCR3-induced migration.

167 chanism for the immunosuppressive effects of IL-16 seen in Th2-mediated inflammation.

168 The effects of IL-16 were blocked by CCR3 inhibitors (met-RANTES, anti-

169 mononuclear cells through the expression of IL-16.

170 The secreted active form of IL-16 has been detected at sites of TH1-mediated inflamm

171 h constitutes the bioactive secreted form of IL-16.

172 nistic explanation for the known function of IL-16 to inhibit the mixed lymphocyte reaction.

173 edium blocked the up-regulation by GD-IgG of IL-16, implicating the FRAP/mTOR/p70(s6k) pathway in the

174 AP/mTOR/p70(s6k) pathway in the induction of IL-16 expression.

175 The induction of IL-16 protein by IL-1beta can be attenuated with specifi

176 6 chemoattractant activity and inhibition of IL-16 binding to CD4 in vitro.

177 quence-based oligopeptides for inhibition of IL-16 chemoattractant activity and inhibition of IL-16 b

178 o Ser109) was shown to mediate inhibition of IL-16 chemoattractant activity.

179 s IL-1beta, they express very high levels of IL-16 protein and chemoattractant activity, a substantia

180 Thus, serum levels of IL-16, a key chemotactic factor for CD4(+) lymphocytes,

181 nstitutive expression of the pro-molecule of IL-16 has been found in T cells, mast cells, eosinophils

182 Neutralization of IL-16 recruitment to its receptor, using an anti-IL16 an

183 stion and to further study the processing of IL-16, new constructs containing either the C-terminal 1

184 Spontaneous production of IL-16 in synovial lesions impairs the functional activit

185 nt studies we investigated the regulation of IL-16 protein and mRNA expression in CD4+ T cells and de

186 low cytometry, and the concurrent release of IL-16, as detected by ELISA.

187 n and significantly inhibited the release of IL-16.

188 t least partially mediated by the release of IL-16.

189 Deletion of 12 or 22 N-terminal residues of IL-16 had no impact on chemoattractant activity, but MLR

190 The restoration of IL-16 expression resulted in significant CD4+ mononuclea

191 ure of Crohn's disease; however, the role of IL-16 in intestinal inflammation is unknown.

192 It is concluded that the secretion of IL-16 is required for HIV inhibition.

193 ed to a signal peptide are poor secretors of IL-16 and show little if any resistance to HIV.

194 roblasts appear to be an important source of IL-16 and through expression of this molecule may have k

195 issue, CD8+ T cells were the major source of IL-16, a natural ligand of the CD4 molecule that can ane

196 in IL-10 and IFN-gamma, but not TGF-beta or IL-16, as well as a decrease in IL-13 in the bronchoalve

197 iators histamine, PGD(2), LTB(4), CXCL10, or IL-16, each of which can be produced by mast cells and o

198 nhibitory effects induced by either gp120 or IL-16 on CCR5.

199 erleukin [IL]-1beta, IL-5, IL-7, IL-12(p70), IL-16, IL-17, IL-20, IL-21, IL-28A, tumor necrosis facto

200 a signal peptide, but with a signal peptide IL-16 is processed through the endoplasmic reticulum-gol

201 he lack of circulating CD8+ T cells prevents IL-16 expression, impairs CD4+ mononuclear cell recruitm

202 Pro-IL-16 comprises a C-terminal cytokine domain and an N-te

203 Pro-IL-16 decreases p27(KIP1) degradation by reducing transc

204 Pro-IL-16 expressed in transfected tumor cells was previousl

205 Pro-IL-16 is a PDZ domain-containing protein expressed in T

206 Pro-IL-16 is a substrate for caspase-3, and cleavage by this

207 The precursor for IL-16 (pro-IL-16) is a nuclear and cytoplasmic PDZ domain-containin

208 d constitutive IL-16 mRNA expression and pro-IL-16 protein in CD4+ and CD8+ T cells.

209 ing and tissue distribution of IL-16 and pro-IL-16, we investigated the distribution of IL-16 mRNA an

210 Because pro-IL-16 is cleaved to its bioactive mature form by caspase

211 led to loss of nuclear translocation by pro-IL-16 and subsequent increases in Skp2 levels and decrea

212 that upon activation of normal T cells, pro-IL-16 mRNA and protein are diminished in close correlati

213 Total cellular pro-IL-16 protein also fell, reaching a nadir at 48 h.

214 ve caspase-3 that is capable of cleaving pro-IL-16, whereas CD4+ T cells require activation for the a

215 We examined pro-IL-16 mRNA and protein expression in resting and anti-CD

216 27(KIP1) levels and implicate a role for pro-IL-16 in T cell proliferation.

217 rated that HDAC activity is critical for pro-IL-16-induced cell cycle arrest.

218 Human pro-IL-16 is comprised of 631 amino acids with three PDZ dom

219 Taken together, these findings identify pro-IL-16 as a novel regulator of Skp2 expression and p27(KI

220 Ectopic expression of pro-IL-16 in pro-IL-16-negative Jurkat cells blocks cell cycle progressio

221 sized as a precursor molecule of 68 kDa (pro-IL-16) that is processed by caspase-3, a member of the I

222 approximately 80-kDa precursor molecule, pro-IL-16.

223 identical with splenocyte-derived mouse pro-IL-16.

224 -ALL), demonstrated reduction in nuclear pro-IL-16 levels.

225 how that N-terminal to the NLS domain of pro-IL-16 are protein kinase CK2 substrate and cdc2 kinase s

226 The nuclear localization signal of pro-IL-16 consists of a classical bipartite nuclear targetin

227 ate that loss of nuclear localization of pro-IL-16 facilitates CTCL cell proliferation by causing a d

228 Ectopic expression of pro-IL-16 in pro-IL-16-negative Jurkat cells blocks cell cyc

229 we show that the N-terminal prodomain of pro-IL-16 translocates into the nucleus following cleavage o

230 16, a domain required for association of pro-IL-16 with the nuclear chaperone HSC70 (also known as HS

231 ions in the 5' end of the PDZ1 region of pro-IL-16, a domain required for association of pro-IL-16 wi

232 nd to the first and second PDZ domain of pro-IL-16, respectively.

233 which regulates nuclear localization of pro-IL-16.

234 quence (NLS) in the N-terminal domain of pro-IL-16.

235 lytic release of the third PDZ domain of pro-IL-16.

236 etylase 3 (HDAC3) as binding partners of pro-IL-16.

237 creted C-terminus of a larger precursor, pro-IL-16.

238 h is cleaved from the precursor protein (pro-IL-16) by caspase-3.

239 rt, by mutations in the scaffold protein pro-IL-16, which directly regulates Skp2 synthesis.

240 nuclear presence of the scaffold protein pro-IL-16.

241 rine and human IL-16 precursor proteins (pro-IL-16).

242 Consistent with the microarray reports, pro-IL-16 mRNA levels fell within 4 h of activation, and thi

243 pases and granzyme B, we determined that pro-IL-16 cleavage is mediated only by caspase-3.

244 aken altogether, these data suggest that pro-IL-16 forms a complex with GABPbeta1 and HDAC3 in suppre

245 In this study we have found that pro-IL-16 is absent or mutated in four T lymphoblastic leuke

246 t on cell cycle progression suggest that pro-IL-16 is cleaved into two functional proteins, a C-termi

247 We further showed that pro-IL-16 is located in a GABP transcriptional complex bound

248 alcineurin-dependent mechanism, and that pro-IL-16 might influence T cell cycle regulation, although

249 These data demonstrate that pro-IL-16 mRNA and protein expression are dynamically regula

250 In addition, we showed that pro-IL-16 regulates the transcription of Skp2, the mechanism

251 as revealed a novel mechanism with which pro-IL-16 regulates T cell growth through the Skp2-p27KIP1 p

252 RA-IgG-provoked IL-16 and RANTES production also appears to involve the

253 RA-IgG-provoked IL-16 expression is inhibited by rapamycin, a specific m

254 uggesting similar conservation of a putative IL-16 binding site on CD4.

255 Moreover, CD8(-/-) mice displayed reduced IL-16 expression and decreased CD4+ T-cell recruitment a

256 CD4+ T cells release IL-16 protein following antigenic stimulation, and this

257 al 100 aa linked to a signal peptide secrete IL-16 and are resistant to HIV replication.

258 Secreted IL-16 contains a characteristic PDZ domain.

259 pase-3, resulting in the release of secreted IL-16.

260 und disruption of putative tumor suppressors IL-16 and translocated promoter region (TPR) in Tax-immo

261 ides containing native or mutated C-terminal IL-16 sequences were tested for IL-16 inhibition.

262 sumed that CD4 is the sole receptor and that IL-16 induces a comparable migratory response in all CD4

263 We now demonstrate that IL-16 preferentially induces migration in a CD25(+)CTLA-

264 We further demonstrate that IL-16-recruited cells are enriched for Forkhead box P3 (

265 In this study we demonstrate that IL-16/CD4 induced receptor desensitization of CXCR3 on p

266 These studies demonstrate that IL-16/CD4 signaling in T lymphocytes also results in los

267 These studies demonstrate that IL-16/CD4 signaling in T lymphocytes results in a select

268 In this study, we determined that IL-16 preferentially induces a migratory response in Th1

269 lls from CCR5(null) mice, we determined that IL-16-induced migration was significantly greater in the

270 mutated forms of CD4, it was determined that IL-16/CD4 induces a p56(lck)-dependent inhibitory signal

271 mutated forms of CD4, it was determined that IL-16/CD4 induces a p56lck-dependent signal that results

272 In addition, we find that IL-16 stimulation may facilitate de novo induction of Fo

273 Recently, it was reported that IL-16 is synthesized as an approximately 80-kDa precurso

274 Here we show that IL-16 is also constitutively present in >98% of freshly

275 h brefeldin A and/or tunicamycin showed that IL-16 is secreted despite the absence of a signal peptid

276 Previous work has shown that IL-16/CD4 induces desensitization of both CCR5- and CXCR

277 These results suggest that IL-16 can prime CD4+ T cells for IL-2 responsiveness, an

278 Prior DNA microarray studies suggested that IL-16 mRNA levels decrease following T cell activation,

279 the placental systems in PE, suggesting that IL-16 could be an important cytokine engaged in the alte

280 This suggests that IL-16 provides an autocrine function in the brain.

281 spread in mice infected with H129wt and the IL-16-expressing recombinant virus.

282 Cerebellar granule neurons express the IL-16 receptor CD4.

283 body requires a conformational change in the IL-16 PDZ domain.

284 also show that the nuclear targeting of the IL-16 prodomain induces a G(0)/G(1) arrest in the cell c

285 Our study demonstrated up-regulation of the IL-16 profile in both the maternal and the placental sys

286 Therefore, IL-16 activation of eosinophils is CD4-mediated to elici

287 Exposure of these cells to IL-16 induces expression of the immediate-early gene, c-

288 eins VEGF, HGF, FGF-2, KL, FLT3 ligand, TPO, IL-16, IGF-1, transforming growth factor-beta1 (TGF-beta

289 , prevented the desensitization of CXCR3 via IL-16/CD4, which was restored after reloading of cholest

290 ed in inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNB

291 of apoptosis in monocytes, we asked whether IL-16 release occurs in monocytes that undergo spontaneo

292 e aim of this study was to determine whether IL-16 production is increased in inflammatory bowel dise

293 mulation, prompted us to investigate whether IL-16 could also alter CXCR4 signaling.

294 associated with CD4, we investigated whether IL-16/CD4 stimulation was enhanced in the presence of CC

295 We evaluated the means by which IL-16, a recognized eosinophil chemoattractant, might ac

296 ntial component of which can be blocked with IL-16-neutralizing Abs.

297 y treating synovium-SCID mouse chimeras with IL-16.

298 ture of the 14.1Fab fragment in complex with IL-16, revealing that binding of the antibody requires a

299 Potential interaction of this domain with IL-16 was studied by testing murine D4 sequence-based ol

300 ata indicate that receptor interactions with IL-16 that activate T cell migration are not identical w

301 Supplemental therapy with IL-16 may be a novel and effective treatment for rheumat