ライフサイエンスコーパス: lymphocyte activation

1 re capable of diminishing IL-18-mediated CD4 lymphocyte activation.

2 e only antigen-specific interaction during T lymphocyte activation.

3 ance of PKC localization for IS dynamics and lymphocyte activation.

4 Semaphorin 7a (Sema 7a) participates in lymphocyte activation.

5 +) T lymphocytes and is downregulated upon T lymphocyte activation.

6 a transcriptional signature indicative of B lymphocyte activation.

7 s-presentation is sufficient for cytotoxic T lymphocyte activation.

8 ortant for proviral genome transcription and lymphocyte activation.

9 isruption of the NFAT pathway and subsequent lymphocyte activation.

10 otein CARMA1 is required for the TCR-induced lymphocyte activation.

11 a) is a novel PKC that plays a key role in T lymphocyte activation.

12 ion (STAT) pathway and play pivotal roles in lymphocyte activation.

13 es to limited oxygen but also are induced by lymphocyte activation.

14 naling microclusters are a common feature of lymphocyte activation.

15 re chronic viral infections, and defective T-lymphocyte activation.

16 f Cdk5-p35 expression that is required for T lymphocyte activation.

17 nal transduction with an important role in T lymphocyte activation.

18 for AIDS progression than was viral load or lymphocyte activation.

19 erly modulate the function and the extent of lymphocyte activation.

20 the major coreceptor of HIV-1, costimulate T lymphocyte activation.

21 e cell migration to draining lymph nodes and lymphocyte activation.

22 ependent increases in soluble CD25 reflected lymphocyte activation.

23 C) is a novel PKC that plays a key role in T lymphocyte activation.

24 aining elevated cytosolic Ca2+ levels during lymphocyte activation.

25 ease-activated Ca2+ channels is required for lymphocyte activation.

26 eir central and peripheral tolerance or in T lymphocyte activation.

27 drugs may disrupt self-tolerance, leading to lymphocyte activation.

28 HIF1alphaI.1 is a negative regulator of lymphocyte activation.

29 tive data providing mechanistic insight into lymphocyte activation.

30 ess CD28, the key costimulatory molecule for lymphocyte activation.

31 cytokinesis, focal adhesion disassembly, and lymphocyte activation.

32 different apoptosis inhibitors often impairs lymphocyte activation.

33 stive protease, did not affect the induced B lymphocyte activation.

34 ck on tumorous tissues via the H2O2-mediated lymphocyte activation.

35 an immunomodulatory molecule induced during lymphocyte activation.

36 , both of which are negative regulators of T-lymphocyte activation.

37 ressive drugs that could specifically dampen lymphocyte activation.

38 nts a novel link between innate immunity and lymphocyte activation.

39 ls, after their deamidation by TG2, induce T-lymphocyte activation accompanied by autoantibody produc

40 H chain (4F2 Ag, Slc3a2) was discovered as a lymphocyte-activation Ag.

41 previous observation in the requirement for lymphocyte activation and argue a revisit of the traditi

42 (k/k) protected Tlr7tg mice from spontaneous lymphocyte activation and autoantibody production.

43 olemic mice, increasing ApoA-I can attenuate lymphocyte activation and autoimmunity in SLE independen

44 g and cell death in preventing inappropriate lymphocyte activation and autoimmunity.

45 ubiquitin chain assembly complex (LUBAC) in lymphocyte activation and B-cell malignancy.1 These data

46 kin-4 (IL-4)-stimulated immune response of B-lymphocyte activation and cell proliferation.

47 ion, cellular ion homeostasis, leukocyte and lymphocyte activation and chemotaxis, protein transport,

48 ed processes, including cytokine production, lymphocyte activation and chemotaxis.

49 vels of Daf1 were correlated with markers of lymphocyte activation and cytokine production.

50 ulate not only lymphocyte apoptosis but also lymphocyte activation and development.

51 ntial role of this regulatory mechanism in T lymphocyte activation and effector function.

52 amily tyrosine kinases are key regulators of lymphocyte activation and effector function.

53 Ca(2+) is crucial for peripheral T-lymphocyte activation and effector functions, and influe

54 and ceramide homeostasis and participate in lymphocyte activation and eosinophil recruitment.

55 uiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive imm

56 and reorganization, which are essential for lymphocyte activation and function.

57 h differential progression and implicated in lymphocyte activation and function.

58 ype animals, coupled with significantly less lymphocyte activation and IFN-alpha production.

59 findings reveal a role for the LUBAC during lymphocyte activation and in B-cell malignancy.

60 chromatin modifications were compared during lymphocyte activation and in ES cells as well.

61 gand (FasL) can result in poor restraints on lymphocyte activation and in increased susceptibility to

62 ional factor that has an important role in T lymphocyte activation and inflammation.

63 RNA miR-155 has been shown to be involved in lymphocyte activation and is expressed in Epstein-Barr v

64 and within non-lymphocyte cells involved in lymphocyte activation and migration into the airways.

65 Lymphocyte activation and migration involve large-scale

66 t have redefined the role of ERM proteins in lymphocyte activation and migration.

67 contributes to the negative regulation of T-lymphocyte activation and peripheral tolerance.

68 These associations highlight key roles for lymphocyte activation and prioritize specific cytokine p

69 l disease was ameliorated by (i) suppressing lymphocyte activation and proinflammatory cytokine produ

70 Ag recognition induces T lymphocyte activation and proliferation and acquisition

71 anscription factor NF-kappaB is required for lymphocyte activation and proliferation as well as the s

72 Lymphocyte activation and proliferation were assessed in

73 s, reflecting common changes associated with lymphocyte activation and proliferation.

74 The paracaspase MALT 1 is a major player in lymphocyte activation and proliferation.

75 ll functions, including antigen-stimulated T lymphocyte activation and proliferation.

76 ion of TCR signaling and preventing abnormal lymphocyte activation and proliferation.

77 a2+ (CRAC) channels, an essential signal for lymphocyte activation and proliferation.

78 riggers a cascade of events that result in T lymphocyte activation and promote positive and negative

79 , paradigm for lncRNA-mediated modulation of lymphocyte activation and signaling, with implications f

80 of apoptotic bodies leading to dysregulated lymphocyte activation and signs of systemic autoimmunity

81 NFSF13) are important regulatory factors for lymphocyte activation and survival in mammals.

82 in their accumulation and, in turn, chronic lymphocyte activation and systemic autoimmune manifestat

83 lar location for protein expression during B lymphocyte activation and the DNA damage response.

84 4) is required during an immune response for lymphocyte activation and the generation of immunoglobul

85 rom the plasma but, in addition, modulates T-lymphocyte activation and the inflammatory response by d

86 protein expression as a function of human T lymphocyte activation and time.

87 ed to cell proliferation in cluster 1 and to lymphocyte activation and unfolded protein responses in

88 l nervous system contributes to peripheral T-lymphocyte activation and vascular inflammation in this

89 sease as well as lymphadenopathy, polyclonal lymphocyte activation, and accelerated memory T cell for

90 iciency virus type 1 (HIV-1) reservoir size, lymphocyte activation, and CCR5 expression in 114 CCR5(D

91 ient mice had ameliorated disease, decreased lymphocyte activation, and decreased serum IgG.

92 These include antigen mimicry, polyclonal lymphocyte activation, and infection-mediated innate end

93 playing crucial roles in stem cell renewal, lymphocyte activation, and leukemogenesis.

94 tration by monocyte-macrophages, decreased T lymphocyte activation, and reduced myocardial damage dur

95 n of Jurkat T-cell attachment, inhibition of lymphocyte activation, and release of inflammatory cytok

96 it is required for embryonic development, T-lymphocyte activation, and resistance to necrosis induce

97 d in inflammation, cytokine signaling, and T-lymphocyte activation, and suppression of genes involved

98 dogenous DC-HIL is a negative regulator of T lymphocyte activation, and that this native inhibitory f

99 ene expression during embryonic development, lymphocyte activation, and tumorigenesis.

100 erated via modulation of CD11c+ APC-mediated lymphocyte activation, and was associated with a decreas

101 omprising a mutant mouse CD80 (CD80w88a) and lymphocyte activation antigen-3 was engineered to concur

102 munology is that metabolic reprogramming and lymphocyte activation are intricately linked.

103 on-induced suppression of cytotoxic CD8(+) T-lymphocyte activation as a tumour-promoting mechanism.

104 cSRS2 induced potent memory CD4+- and CD8+-T-lymphocyte activation, as indicated by proliferation and

105 K, two Tec kinases activated downstream of T-lymphocyte activation, both of which are up-regulated in

106 ay is critical for antigen receptor-mediated lymphocyte activation, but its function in cytokine sign

107 vement of immunoreceptor microclusters tunes lymphocyte activation, but the underlying mechanisms are

108 T lymphocyte activation by antigen conditions adaptive imm

109 fect of PD-1 engagement and ICOS blockade on lymphocyte activation by in vitro T-cell proliferation a

110 indicate that the Lck SH3 domain controls T lymphocyte activation by regulating MAPK pathway inducti

111 whole-organ imaging and spatially controlled lymphocyte activation by s.c. administered antibodies in

112 , largely orchestrate memory CD8(+) T and NK lymphocytes activation by differentiating into interleuk

113 T-lymphocyte activation can be targeted by blocking co-sti

114 uring respiratory-virus infection, excessive lymphocyte activation can cause pathology both in acute

115 However, another subgroup had lymphocyte activation comparable with that in uninfected

116 hat both massive lymphocytosis and excessive lymphocyte activation could contribute to massive cytoki

117 Both massive lymphocytosis and excessive lymphocyte activation could contribute to massive cytoki

118 Furthermore, lymphocyte activation creates an environment favorable t

119 2ME2 inhibits in vitro lymphocyte activation, cytokine production, and prolifer

120 c mechanisms, including microbe recognition, lymphocyte activation, cytokine signaling, and intestina

121 T lymphocyte activation decreased the requirement for pO(2

122 Many patients with SCID have lymphocyte-activation defects that remain uncharacterize

123 late in infection, suggesting that there is lymphocyte activation despite substantial bystander apop

124 lupus pathology by broadly affecting T and B lymphocyte activation/differentiation.

125 Aberrant T lymphocyte activation due to signaling abnormalities, li

126 However, the role of C5a in innate lymphocyte activation during sepsis remains elusive.

127 engagement is critically required for normal lymphocyte activation during the adaptive immune respons

128 tor signaling is required for normal B and T lymphocyte activation during the adaptive immune respons

129 ent is a highly regulated event required for lymphocyte activation during the adaptive immune respons

130 As PD-L1 functions to fine tune lymphocyte activation, dysregulation of cytokines result

131 Lymphocyte activation following pristane injection was g

132 a highly specific event such antigen-driven lymphocyte activation, for example, polarization to a T

133 These cytokines are integral to lymphocyte activation, function, and proliferation.

134 summarizes current experimental evidence of lymphocytes' activation, functional role, and crosstalk

135 The inhibitory molecule lymphocyte activation gene 3 (LAG-3) and metalloprotease

136 fested by programmed cell death 1 (PD-1) and lymphocyte activation gene 3 (LAG-3) expression and a la

137 Lymphocyte activation gene 3 (LAG-3) is a CD4-related, a

138 o be involved in Treg modulation of DC, with lymphocyte activation gene 3 (LAG-3) playing a predomina

139 ), granzyme B, and CD107a and a reduction in lymphocyte activation gene 3 (LAG-3), programmed cell de

140 ltiple inhibitory receptors, including PD-1, lymphocyte activation gene 3 (LAG-3), T cell Ig mucin 3,

141 cells, such as programmed death 1 (PD-1) and lymphocyte activation gene 3 (LAG-3).

142 rkers programmed death receptor 1 (PD-1) and lymphocyte activation gene 3 (Lag-3).

143 was important to their induction of CD25(+) lymphocyte activation gene 3 (LAG3)(+), CD49b(-), forkhe

144 glucocorticoid-induced TNF receptor [GITR], lymphocyte activation gene 3 [LAG3]), TH1/TH2 cytokines,

145 ell markers (forkhead box protein 3 [FOXP3], lymphocyte activation gene 3 [LAG3], and glucocorticoid-

146 IL-10, inducible T-Cell costimulator (ICOS), lymphocyte activation gene 3 protein (LAG-3), and CD49b,

147 sion patterns for several markers, including lymphocyte activation gene 3, KLRG1, CD103, ICOS, CTLA-4

148 Despite expressing the cell surface Ags lymphocyte activation gene-3 (CD223) and CD103, neither

149 Lymphocyte activation gene-3 (LAG-3) is a CD4-related tr

150 Lymphocyte activation gene-3 (LAG-3) is a cell-surface m

151 Lymphocyte Activation Gene-3 (LAG-3) is a transmembrane

152 sion of programmed death ligand-1 (PD-1) and lymphocyte activation gene-3 (LAG-3) receptors were freq

153 luating the benefits of systemic blockade of lymphocyte activation gene-3 (LAG-3) signals to improve

154 ytotoxic T-lymphocyte attenuator-4 (CTLA-4), lymphocyte activation gene-3 (LAG-3), and programmed dea

155 D-1), T cell immunoglobulin mucin-3 (TIM-3), lymphocyte activation gene-3 (LAG-3), cytotoxic T-lympho

156 Lymphocyte activation gene-3 (LAG-3; CD223) is a CD4 hom

157 Lymphocyte activation gene-3 (LAG3) (CD223) is the third

158 tio, 8.7; confidence interval, 2.4-31.2) and lymphocyte activation gene-3 (odds ratio, 3.3; confidenc

159 xpress high levels of programmed death-1 and lymphocyte activation gene-3 and modestly suppress the p

160 Tregs were activated in vivo, and when using Lymphocyte Activation Gene-3 as a selection marker, as f

161 e CD160, B- and T-lymphocyte attenuator, and lymphocyte activation gene-3 inhibitory pathways.

162 , including T-cell-related transcripts CD25, lymphocyte activation gene-3, Granzyme B, and interleuki

163 osts encode an additional CD4 family member, lymphocyte activation gene-3, which is a marker for acti

164 ed Programmed Death-1, CD160 and 2B4 but not lymphocyte activation gene-3.

165 immune regulation, including TGF-beta(3) and lymphocyte activation gene-3.

166 domain molecule of CD4 and the related gene, lymphocyte activation gene-3.

167 Lymphocyte-activation gene 3 (LAG-3) is an immune inhibi

168 Accordingly, they upregulate lymphocyte-activation gene 3 (LAG-3), T cell immunoglobu

169 ed cell death 1 (PD-1; also known as CD279), lymphocyte-activation gene 3 (LAG-3; also known as CD223

170 Lymphocyte-activation gene 3 (LAG3) is a protein with a

171 re characterized by the presence of CD49b(+) lymphocyte-activation gene 3 (LAG3)(+) TR1 cells, antige

172 Here, we show that LAG3 (lymphocyte-activation gene 3) binds alpha-syn PFF with h

173 molecule dual blockade (anti-PD-L1 and anti-lymphocyte-activation gene 3) increased the number of ci

174 e expression (e.g., programmed cell death 1, lymphocyte-activation gene 3, and 2B4) and diminished Ag

175 -1 (PD-1) alone and PD-1 in combination with lymphocyte-activation gene-3 (LAG-3).

176 The third cluster was enriched in lymphocyte activation genes and was associated with a hi

177 e production, and reduced expression of many lymphocyte activation genes.

178 histone methyltransferase Ezh2 in regulating lymphocyte activation has been suggested, but the molecu

179 in response to TCR ligation, but its role in lymphocyte activation has not been addressed.

180 eutic potential of costimulatory signals for lymphocyte activation have spurred a large amount of wor

181 We observed that LTA potently suppressed T-lymphocyte activation in a Toll-like receptor 2-independ

182 und to play a surprisingly prominent role in lymphocyte activation in addition to its well-known role

183 We also evaluated the kinetics of T-lymphocyte activation in both the systemic and the mucos

184 A striking but transient T-lymphocyte activation in both the systemic and the mucos

185 ominent increase in viral loads and CD4(+) T lymphocyte activation in controllers than in progressors

186 l blockade of this channel inhibits VSMC and lymphocyte activation in rats and mice.

187 BP production is a reduction in CD4-positive lymphocyte activation in response to IL-18 costimulation

188 mice exhibit a heightened state of CD4(+) T lymphocyte activation in the chronic phase of infection

189 gamma significantly promotes recruitment and lymphocyte activation in the earliest phases of autoimmu

190 ghlight a local shift in gene expression and lymphocyte activation in the ZAM.

191 in herniated IVDs suggests a pattern of Th1 lymphocyte activation in this pathology.

192 To assess the role of KCa3.1 channels in lymphocyte activation in vivo, we studied T cell functio

193 g complexes are dynamically regulated during lymphocyte activation in vivo.

194 ly significant and sensitive marker of early lymphocyte activation in vivo.

195 lymphoma b (Cbl-b), a negative regulator of lymphocyte activation, in tumor-reactive CD8(+) T cells

196 d higher expression of genes associated with lymphocyte activation, including the Th1 and Th17-relate

197 Chronic lymphocyte activation is commonly present in the CNS of

198 Moreover, lymphocyte activation is impaired in C57BL/6 mice that e

199 Lymphocyte activation is initiated by a global increase

200 As lymphocyte activation is involved in the pathogenesis of

201 nisms, but their genome-wide regulation of T lymphocyte activation is largely unknown.

202 Lymphocyte activation is regulated by costimulatory and

203 down-regulation of CD62L that accompanies T lymphocyte activation is thought to redirect cells away

204 prolonged activation of IP(3)R1 required for lymphocyte activation is unclear.

205 signaling to NF-kappaB, essential for normal lymphocyte activation, is dysregulated in several types

206 sult in decreased antigen presentation and T-lymphocyte activation, leading to incomplete and/or weak

207 on, suggesting that apoptosis induction upon lymphocyte activation limits cellular and humoral immune

208 papillary cell RCC aberrantly expressing the lymphocyte activation marker CD70, a member of the tumor

209 tion led to a reduction in the expression of lymphocyte activation markers and resulted in reduced cy

210 ncreased expression of certain platelets and lymphocytes activation markers in chronic HCV and S. man

211 studies suggested that certain platelets and lymphocytes activation markers may have an impact on pro

212 T-lymphocyte activation may contribute to atherosclerosis,

213 sociated with a greater increase in CD4(+) T lymphocyte activation (measured by Ki-67 expression) in

214 ddition to the primary MV receptor signaling lymphocyte activation molecule (SLAM or CD150), we asked

215 stably expressing the MV receptor signaling lymphocyte activation molecule (SLAM or CD150).

216 cated immune cell receptors of the signaling lymphocyte activation molecule (SLAM) family during host

217 The signaling lymphocyte activation molecule (SLAM) family includes ho

218 key homotypic interactions between signaling lymphocyte activation molecule (SLAM) family members.

219 Ly108 (CD352) is a member of the signaling lymphocyte activation molecule (SLAM) family of receptor

220 d on cell surface markers from the signaling lymphocyte activation molecule (SLAM) family of receptor

221 The signaling lymphocyte activation molecule (SLAM) family of receptor

222 ive B and T cells interact via the signaling lymphocyte activation molecule (SLAM) family receptor, S

223 s (RNA-ICs), the expression of the signaling lymphocyte activation molecule (SLAM) family receptors C

224 -gamma-producing T cells expressed signaling lymphocyte activation molecule (SLAM), and SLAM activati

225 sed by the absence of a functional signaling lymphocyte activation molecule (SLAM)-associated protein

226 The signaling lymphocyte activation molecule (SLAM)-associated protein

227 CD4(+) T cells deficient in signaling lymphocyte activation molecule (SLAM)-associated protein

228 Signaling lymphocyte activation molecule (SLAM)-associated protein

229 /SAP, an adaptor that recruits Fyn to signal lymphocyte activation molecule (SLAM)-related receptors.

230 is virus is the immune cell marker signaling lymphocyte activation molecule (SLAM).

231 e expressing the MV receptor human signaling lymphocyte activation molecule (SLAM, CD150) with human-

232 BACKGROUND & AIMS: Signaling lymphocyte activation molecule (Slamf)1 is a co-stimulat

233 aired induction and maintenance of signaling lymphocyte activation molecule 6 expression, a TCR costi

234 induce PLZF, in part by regulating signaling lymphocyte activation molecule 6 expression.

235 The signaling lymphocyte activation molecule F1 (SLAMF1) is both a mic

236 leukocyte immunoglobulin-like and signalling lymphocyte activation molecule families and a number of

237 Signaling lymphocyte activation molecule family (SLAMF)2/CD48 is a

238 inted to an important role for the signaling lymphocyte activation molecule family (slamf)6 surface r

239 CD84 belongs to the signaling lymphocyte activation molecule family of immunoreceptors

240 function of the mouse glycoprotein Signaling Lymphocyte Activation Molecule Family receptor (SLAMF) 4

241 le-positive thymocytes through the signaling lymphocyte activation molecule family receptor Ly108 mar

242 ters act as positive regulators of signaling lymphocyte activation molecule family receptor-specific

243 ind to phosphorylated tyrosines of signaling lymphocyte activation molecule family receptors in murin

244 KT cells and mediates signals from signaling lymphocyte activation molecule receptors that are exclus

245 philic immunoreceptor of the SLAM (signaling lymphocyte activation molecule) family-on either platele

246 er (PLZF) and the adaptor molecule signaling lymphocyte activation molecule-associated protein (SAP)

247 Signaling lymphocyte activation molecule-associated protein (SAP)

248 d phagocytosis was independent of signalling lymphocyte activation molecule-associated protein (SAP)

249 utations in SH2D1A (Xq25) encoding signaling lymphocyte activation molecule-associated protein (SAP),

250 el, loss-of-function mutations in signalling lymphocyte activation molecule-associated protein (SAP,

251 s-linking, and relative paucity of signaling lymphocyte activation molecule-associated protein promot

252 ing lymphocyte activation molecule/signaling lymphocyte activation molecule-associated protein signal

253 nificant role in the regulation of signaling lymphocyte activation molecule-associated protein-mediat

254 cell development is controlled by signaling lymphocyte activation molecule/signaling lymphocyte acti

255 s were used to infect Vero or Vero/signaling lymphocyte-activation molecule (SLAM) cells in PRN assay

256 on is 2B4 (CD244), a member of the signaling lymphocyte-activation molecule (SLAM) family that binds

257 idence suggests a crucial role for signaling lymphocyte activation molecules (SLAMs) in the expressio

258 Signaling lymphocyte activation molecules (SLAMs) play an integral

259 d to evaluate the potential of platelets and lymphocytes activation molecules expression on the patho

260 Marked lymphocyte activation occurred immediately postinfection

261 aft rejection diseases, in which a sustained lymphocyte activation occurs in the presence of persiste

262 Infiltration of T lymphocytes, activation of microglia, and their interpla

263 ed increased expression of CD69, a marker of lymphocyte activation, on diabetic T-cells.

264 siRNA-fusion protein complexes do not cause lymphocyte activation or induce IFN responses.

265 line of CD4(+) T cells, a robust increase in lymphocyte activation, or change in the level of SIV-spe

266 (fl/fl)Cd4(Cre) mice resulted in spontaneous lymphocyte activation, primarily due to numerical and fu

267 To identify new suppressors of lymphocyte activation, proliferation, and function, we e

268 s receptor indicate that IL-21 has a role in lymphocyte activation, proliferation, differentiation, a

269 MHC activation potency, suggesting that full lymphocyte activation required a minimal lifetime for TC

270 T lymphocyte activation requires signal 1 from the TCR and

271 ed levels of corticosterone, which modulates lymphocyte activation responses and apoptosis during str

272 atment with Con A in a model of polyclonal T lymphocyte activation resulted in a greatly enhanced Th1

273 We have only recently begun to examine lymphocyte activation's relationship to adaptive immunit

274 tol 4,5-biphosphate (PIP2) is critical for T lymphocyte activation serving as a substrate for the gen

275 This was the only fraction to induce B-lymphocyte activation, since all the other fractions fai

276 cts gene expression in a manner dependent on lymphocyte activation status, contributing to the interi

277 Drug lymphocyte activation test (LAT) was conducted by measur

278 mal, scratch, and/or patch tests, as well as lymphocyte activation tests (LATs).

279 Moreover, results of lymphocyte activation tests showed the absence of drug-s

280 munohistochemistry, RT-qPCR, flow cytometry, lymphocyte activation tests, and different cell-free pro

281 ellular and molecular mechanisms following B lymphocyte activation that lead to IgM secretion are not

282 monstrate that loss of CD47 causes increased lymphocyte activation that results in increased atherosc

283 ough zeta-chain is critically important in T lymphocyte activation, the mechanism of the decreased ze

284 In particular, lymphocyte activation thresholds are subject to tuning,

285 Selective inhibition of lymphocyte activation through abrogation of signal 3-cyt

286 Immune tolerance prevented cytotoxic T lymphocyte activation to F.IX and CD8(+) cellular infilt

287 Lymphocyte activation triggers adhesiveness of lymphocyt

288 ncent Allfrey and colleagues discovered that lymphocyte activation triggers massive acetylation of ch

289 gut, and their expression is induced during lymphocyte activation under the influence of retinoic ac

290 rinsic feedback control mechanism to balance lymphocyte activation upon antigenic stimulation.

291 T lymphocyte activation, Vbeta expansion, and IFN-gamma re

292 The ezrin-radixin-moesin proteins regulate B lymphocyte activation via their effect on BCR diffusion

293 T-cell-associated HIV-1 DNA and RNA levels, lymphocyte activation, viral population structure, and v

294 Furthermore, DC-dependent T-lymphocyte activation was blocked by anti-CD86 antibody

295 Lymphocyte activation was examined using flow cytometry,

296 Lymphocyte activation was normal, as demonstrated by nor

297 ecause FDCs provide signaling that increases lymphocyte activation, we postulated that FDCs could inc

298 d blast formation as a readout of specific T lymphocyte activation, we report the presence in M. tube

299 In metastatic LNs, signs of B lymphocyte activation were observed, as evidenced by inc

300 ession levels, also an established marker of lymphocyte activation, were significantly increased on M