ライフサイエンスコーパス: lymphocyte

1 testinal epithelium and among lamina propria lymphocytes.

2 mediating V(D)J recombination in developing lymphocytes.

3 NKT) cells, a specialized subset of innate T lymphocytes.

4 elopment, activation, and differentiation of lymphocytes.

5 to pathogenesis by activating auto-reactive lymphocytes.

6 munomodulatory threshold in murine and human lymphocytes.

7 an immune response from CD4(+) and CD8(+) T lymphocytes.

8 tically dependent on central memory CD8(+) T lymphocytes.

9 r cytotoxicity compared with other cytotoxic lymphocytes.

10 for the enumeration and characterization of lymphocytes.

11 enabled tumor debulking by tumor-redirected lymphocytes.

12 reduction in the number of tumor cytotoxic T lymphocytes.

13 esenting immunogenic peptides to cytotoxic T lymphocytes.

14 ubsets while decreasing CD103(+) and CD69(+) lymphocytes.

15 orm a tailored adaptive response via T and B lymphocytes.

16 ltrating lymphocytes (TIL) and intra-hepatic lymphocytes.

17 apex of the hierarchical system of memory T lymphocytes.

18 a heterogeneous population of infiltrating T lymphocytes.

19 ver (Ag) in individual Ag NP exposed human T-lymphocytes.

20 ched by Nkrp1g on subsets of intraepithelial lymphocytes.

21 equencies of macrophages, neutrophils, and T lymphocytes.

22 strategy to enhance the generation of memory lymphocytes.

23 cancer cells in response to the activated T-lymphocytes.

24 some activity conferred attributes of memory lymphocytes.

25 less abundantly, in neutrophils, but not in lymphocytes.

26 umber of hematopoietic lineages, including T lymphocytes.

27 rom murine T helper type 17-differentiated T lymphocytes.

28 is essential for the development of B and T lymphocytes.

29 us dendritic cells and even tumor-reactive T lymphocytes.

30 shedding of Syndecan-4 from the surface of B-lymphocytes.

31 suppressor of antigen receptor signaling in lymphocytes.

32 antigens by dendritic cells (DCs) to naive T lymphocytes.

33 an increased level of apoptosis in patients' lymphocytes, a decrease in mitochondrial respiration in

34 Depletion of CD4(+) or CD8(+) T lymphocytes abolished this growth inhibition, identifyin

35 nvolved in facilitating diapedesis of CD4(+) lymphocytes across both types of MVECs, whereas ERK was

36 We demonstrate that B-lymphocytes activated by un-methylated CpG motifs, found

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 and T-cell markers were assessed in hepatic lymphocytes after ischemia reperfusion injury (IRI) in h

53 reduction strategy selected three pathways (lymphocyte, alpha-linoleic acid metabolism, IGF regulati

54 rag1 mutant zebrafish, which lack lymphocytes, also form noncaseating granulomas with simi

55 d the proliferation of healthy donor-derived lymphocytes, an effect which was attenuated following se

56 ited reduced kidney leukocyte recruitment (T lymphocytes and classic M1 proinflammatory macrophages)

57 Electron microscopy studies of peripheral lymphocytes and CLN3 transcript analysis with polymerase

58 ated the preferential recruitment of CCR4(+) lymphocytes and CXCR1(+), CXCR2(+), and CCR2(+) myeloid

59 d by antigen-specific interactions between T lymphocytes and dendritic cells (DCs).

60 s affected gut-homing and differentiation of lymphocytes and displayed morphologically in large lymph

61 st engraftment with functional human T and B lymphocytes and human mast cells were found in significa

62 otherapy conditioning regimen depleted blood lymphocytes and increased serum interleukin-15 (IL-15).

63 common gammaherpes virus with tropism for B lymphocytes and infection in immunocompetent individuals

64 The TF BACH2 is essential for T and B lymphocytes and is associated with an archetypal super-e

65 (SOCE) is the main Ca(2+) influx pathway in lymphocytes and is essential for T cell function and ada

66 T lymphocytes and macrophages both display immunosuppressi

67 of phosphorylated STAT1 and STAT3 in patient lymphocytes and monocytes.

68 cterial burden, disorganized accumulation of lymphocytes and mononuclear cells, and extensive pulmona

69 iary subunits on Cav1 alpha1 function in TH2 lymphocytes and on the development of acute allergic air

70 s increases the number of tumor-infiltrating lymphocytes and overall survival after DNA damaging chem

71 Ngamma-producing CD8(+) tumor-infiltrating T lymphocytes and results in a profound extension of the m

72 mpullitis comprising clusters of B (CD21(+)) lymphocytes and significant infiltration of T (CD3(+), C

73 gans that coordinate both the maintenance of lymphocytes and the initiation of immune responses.

74 antify the yield of granulocytes, monocytes, lymphocytes and three subsets of DCs from single human C

75 ifies the population dynamics of neutrophil, lymphocyte, and monocyte characteristics.

76 ogrammed cell death 1 [PD-1] and cytotoxic T-lymphocyte antigen 4 [CTLA-4]) was similar to that of co

77 r T-cell responses by binding to cytotoxic T-lymphocyte antigen 4.

78 imarily secreted by neutrophils, followed by lymphocyte antigen 6 complex(high) monocytes and/or macr

79 dulate the immune responses of monocytes and lymphocytes are not yet well described.

80 Lymphocytes are readily available for research with a la

81 We previously showed that cutaneous lymphocyte-associated antigen (CLA), a functional E-sele

82 mice and involves the contribution of LFA-1 (lymphocyte-associated antigen 1) and alpha4 integrins.

83 e-like anchor protein (LRBA) and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) deficiencies giv

84 emonstrate reduced expression of cytotoxic T lymphocyte-associated genes and IFN-gamma-inducible chem

85 nt inhibitory antibodies against cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and programmed

86 autophagic machinery in DCs in a cytotoxic T-lymphocyte-associated protein 4-dependent (CTLA4-depende

87 entified a subset of CD8(+)PD-1(+)FOXP3(+) T lymphocytes at the earliest phase of functional differen

88 ffector activity more rapidly than wild-type lymphocytes at tumor beds expressing PD-1 ligand (CD274)

89 Vascular endothelium activation and lymphocyte attraction, together with dendritic cell-medi

90 ity and activation of Cav1.2 channels in TH2 lymphocytes both in vitro and in vivo, as demonstrated b

91 rget proinflammatory cytokines produced by T lymphocytes, but the need for improved therapies persist

92 The positive and negative selection of lymphocytes by antigen is central to adaptive immunity a

93 ssing proliferation of CD3- and B220-postive lymphocytes by double immunohistochemistry (PCNA-stainin

94 In addition, activation of CD4(+) T lymphocytes by immune checkpoint blockade increased vess

95 ved that basal metabolic content measured in lymphocytes by nuclear magnetic resonance spectroscopy w

96 The mechanisms through which infiltrating lymphocytes cause disease remain unknown.

97 Consistent with this notion, RT-PCR of lymphocyte cell lines from one of the kindreds showed re

98 d classifiers enable identification of three lymphocyte cell types (B, CD4+ T, and CD8+ T cells) with

99 Identification of lymphocyte cell types are crucial for understanding thei

100 present the identification of non-activated lymphocyte cell types at the single-cell level using ref

101 via effects within ASM cells and within non-lymphocyte cells involved in lymphocyte activation and m

102 euronal density, perivascular CD3-positive T-lymphocyte clustering, and fibrinogen extravasation were

103 n an altered composition of this innate-like lymphocyte compartment.

104 is accomplishable by recruiting cytotoxic T lymphocytes, concomitant with downregulation of Foxp3(+)

105 ood of donors exhibited similar monocyte and lymphocyte content and low serum levels of pro-inflammat

106 An important mechanism of lymphocyte contraction is clonal depletion of activated

107 cidofovir; CR = 13 (80%) vs 8 (35%); median lymphocyte count = 320/mul vs 910/mul; P < .05).

108 Absolute lymphocyte count of <200 cells/mm(3) was associated with

109 Naive lymphocyte counts peaked around 1 year, whereas most mem

110 ne metagene expression values and histologic lymphocyte counts to quantify immune infiltration and as

111 , and negatively associated with post-stroke lymphocyte counts.

112 -specific cross-presentation and cytotoxic T lymphocyte (CTL) activity.

113 CD8(+) cytotoxic T lymphocytes (CTLs) eliminate virally infected cells thro

114 clinical-grade BCR-ABL-specific cytotoxic T lymphocytes (CTLs), endowed with antileukemia activity,

115 plification protocol from PBMCs and enriched lymphocyte cultures.

116 tic infections increases as circulating CD4+ lymphocytes decrease to less than 200 cells/muL; however

117 procal depletion or inactivation of CD4(+) T lymphocytes decreased vessel normalization, indicating a

118 on levels correlate with T regulatory (Treg) lymphocyte densities in the tumor microenvironment.

119 CD8(+) lymphocyte-depleted macaques infected with simian immuno

120 g tolerogenic cytokine administration and/or lymphocyte depletion prior to oral antigen-specific immu

121 tetraprolin-deficient mice after cytotoxic T lymphocyte depletion, but also in WSX-1/tristetraprolin

122 Despite eliciting broader B lymphocyte depletion, continuous combo therapy afforded

123 251-infected macaques with or without CD8(+) lymphocyte depletion.

124 way smooth muscle cells (ASMCs) in vitro via lymphocyte-derived membrane conduits (LMCs) structurally

125 Lymphocyte development and differentiation rely on cytok

126 e CD45.1/CD45.2 congenic system for tracking lymphocyte development.

127 ing microbial infection, responding CD8(+) T lymphocytes differentiate into heterogeneous subsets tha

128 The transcriptional programs that guide lymphocyte differentiation depend on the precise express

129 hanisms by which LFA-1 signaling influence T lymphocyte differentiation into the effector subsets Th1

130 Lymphocyte differentiation is set to produce myriad immu

131 Unfortunately, the B lymphocyte-directed T1D interventions tested to date fai

132 0-23:DQ8 tetramers, stained peripheral blood lymphocytes directly ex vivo, and show DQ8(+) patients w

133 gammadelta T lymphocytes, dominant T cell subsets in the intestine, m

134 However, data on lymphocyte dynamics and the antigen specificity of T cel

135 rogression, preferentially localizing near T lymphocytes early in disease and B cells with advanced d

136 tem (TSCM) cells are a rare subset of memory lymphocytes endowed with the stem cell-like ability to s

137 esponse to enteric infections that modulates lymphocyte energy utilization and dynamics and supports

138 d cell (WBC) counts (neutrophils, monocytes, lymphocytes, eosinophils, basophils) differ by ethnicity

139 maturation is a Darwinian process in which B lymphocytes evolve potent antibodies to encountered anti

140 nce the 1990s it has been known that B and T lymphocytes exhibit low-level, constitutive signaling in

141 tively, animals that were depleted of CD8(+) lymphocytes exhibited greater variation in population dy

142 ling and bioenergetics pathways that mediate lymphocyte exit from quiescence.

143 determined the impact of HCA on the CD4(+) T lymphocyte exometabolome and identified potential biomar

144 Lymphocytes expressing C-X-C chemokine receptor 3 CD8 si

145 atory previously showed that NK and CD8(+) T lymphocytes facilitate the pathobiology of septic shock.

146 , Runx3-deficient CD8(+) tumour-infiltrating lymphocytes failed to accumulate in tumours, resulting i

147 wever, their intrinsic, direct regulation of lymphocyte fate remained unclear.

148 3, and 4 were associated with neutrophil and lymphocyte frequencies and neutrophil/lymphocyte ratio a

149 Lymphocytes from 20 recipients undergoing alemtuzumab-in

150 T lymphocytes from patients carrying constitutive active m

151 Natalizumab inhibits the trafficking of lymphocytes from the blood into the brain and spinal cor

152 vated Ca(2+) (CRAC) channels is critical for lymphocyte function and immune responses.

153 on critically depends on the beta2 integrins lymphocyte function-associated antigen 1 (LFA-1) (CD11a/

154 Lymphocyte function-associated antigen 1 (LFA-1) affinit

155 In latency reservoirs, such as B lymphocytes, gammaHVs exist as viral episomes and expres

156 arrow (BM)-resident (p190)BCR-ABL-specific T lymphocytes has been correlated with hematologic and cyt

157 ancer through the use of ACT with autologous lymphocytes has provided an opportunity to directly inve

158 scovered under the lenses of immunology, and lymphocytes have been implicated in the pathogenesis of

159 Chromosomal aberrations (CAs) in blood lymphocytes have been shown to be associated with overal

160 Nodular lymphocyte Hodgkin lymphoma (NLPHL) is a rare disease fo

161 Intestinal intraepithelial lymphocytes (IELs) are a large and diverse population of

162 clonal population of innate intraepithelial lymphocytes (IELs) lacking classical B-, T-, and natural

163 Here, we describe type 2 innate lymphocytes (ILC2s) as a novel cell type resident in the

164 ng is a hallmark feature of the neoplastic B lymphocytes in chronic lymphocytic leukaemia (CLL).

165 igh-throughput immunological testing of such lymphocytes in combination with improvements in deep seq

166 has great potential to identify Ag-activated lymphocytes in human disease.

167 tated (pATM), were quantified in circulating lymphocytes in operators during the peri-operative perio

168 ys, SGN-CD19B effectively depleted CD20(+) B lymphocytes in peripheral blood and lymphoid tissues con

169 with increased numbers of tumor-infiltrating lymphocytes in primary colon tumors and liver metastases

170 ased numbers of GM-CSF-producing CD4 and CD8 lymphocytes in the blood and joints of patients with spo

171 er through regulatory T cell induction among lymphocytes in the intestinal lamina propria (LPL) and c

172 ase characterized by infiltration of T and B lymphocytes in the pituitary gland.

173 ly including tissue macrophages) and T and B lymphocytes in the presence of detectable inflammatory r

174 The coculture of platelets with lymphocytes in the presence of stimulation decreased the

175 ificantly lower levels of tumor-infiltrating lymphocytes in triple-negative breast cancers and while

176 nvestigating the pathophysiological roles of lymphocytes in various diseases including cancers, autoi

177 or the efficient transformation of primary B lymphocytes in vitro and possibly in vivo The tumor supp

178 cient reduction of the number of circulating lymphocytes in vivo.

179 Only polymyxin B could reduce hepatic lymphocytes in WD-fed FXR KO mice.

180 B-lymphocytes, in addition to their well-known function as

181 in each cell subset and preserves functional lymphocytes, including virus-specific T cells.

182 B-lymphocyte-induced maturation protein 1 (Blimp1) is a tr

183 criptional regulator of PC differentiation B lymphocyte-induced maturation protein-1 (BLIMP-1), and t

184 iroc, confirming the use of CXCR6 in primary lymphocyte infection.

185 ing patients and longer PFS with increased T-lymphocyte infiltrates, irrespective of PD-1 expression.

186 Moreover, an increase of pathogenic lymphocyte infiltration and the secretion of pro-inflamm

187 disruption of vessel normalization reduced T lymphocyte infiltration as expected, reciprocal depletio

188 ith immunostimulatory pathways, especially T lymphocyte infiltration or activity.

189 Epstein-Barr virus (EBV) infection and dense lymphocyte infiltration.

190 ng Abs that inhibit the entry of circulating lymphocytes into lymph nodes and long-term parabiosis ex

191 Infiltration of B lymphocytes into the subepithelial tissue of the lungs h

192 pression of AKAP7 and ITGA3 in primary human lymphocytes is associated with a highly adherent phenoty

193 stematic interrogation of tumor-infiltrating lymphocytes is key to the development of immunotherapies

194 ); however, the pathophysiological role of T lymphocytes is unclear.

195 Human cytotoxic lymphocytes kill intracellular microbes.

196 s9 gene editing revealed that both BTK and B lymphocyte kinase (BLK) are relevant targets of ibrutini

197 of MRN in cancer, we engineered mice with B lymphocytes lacking MRN, or harboring MRN in which MRE11

198 IFN-gamma production by these lymphocytes likely plays a key role in the early control

199 CD8(+) T lymphocytes mediate potent immune responses against tumo

200 suggest that shared risk variants influence lymphocyte-mediated immunity.

201 liver carcinogenesis and induces cytotoxic T-lymphocyte-mediated regression of established hepatocell

202 g) as primarily responsible for defects in B lymphocyte migration and antibody responses that accompa

203 emodeling, induced by okadaic acid, restores lymphocyte migration in response to chemokines, both in

204 egrin LFA-1 is known to play a key role in T lymphocyte migration, which is necessary to mount a loca

205 Little is known about the dynamics of lymphocyte movement in the pancreas during disease progr

206 lative conditioning recipients have better B-lymphocyte/myeloid chimerism and are free from immunoglo

207 common grade 3 adverse events were decreased lymphocyte (n=3) and decreased neutrophil count (n=2); a

208 rized by unbridled activation of cytotoxic T lymphocytes, natural killer (NK) cells, and macrophages

209 ry cells such as infiltrating macrophages, T lymphocytes, neutrophils, and DCs all contribute to live

210 ion that is dependent on neither cytotoxic T lymphocytes nor humoral immune response.

211 nonuclear cell (PBMC) ADA activity, improved lymphocyte numbers, and normal proliferative responses t

212 ence of an inflammatory process initiated by lymphocytes of the immune system.

213 and induce sr39tk expression in platelets, T lymphocytes or cardiomyocytes.

214 rypt depth ratio, numbers of intraepithelial lymphocytes, or serologic markers of celiac disease.

215 ceptor-homologous molecules expressed on TH2 lymphocytes, PDE4, the histamine 4 receptor, and Janus k

216 a TCRalphabeta(+) intestinal intraepithelial lymphocytes play a critical role in promoting intestinal

217 In NOD mice and also likely humans, B lymphocytes play an important role as APC-expanding auto

218 )-mediated inhibition of activated PD-1(+) T lymphocytes plays a major role in tumor escape from immu

219 ts, immunologic analysis of peripheral blood lymphocyte populations by using flow cytometry, and hist

220 el studies highlight the role of innate-like lymphocyte populations in the early inflammatory respons

221 NA sequencing to CD4(+), CD8(+), and CD19(+) lymphocyte populations isolated from 81 subjects with ty

222 ite adipose tissue contained abundant memory lymphocyte populations.

223 characterization and incidence of anti-tumor lymphocytes present in patients with cancer.

224 h T cell clonal dominance among intratumoral lymphocytes prior to treatment or among peripheral T cel

225 is the result of a very fine balance between lymphocyte production, proliferation, and apoptosis.

226 clusion, we show that pituitary-infiltrating lymphocytes proliferate in situ during AH, providing a p

227 ngly, PPTSP44 triggered the highest level of lymphocyte proliferation and IFN-gamma production.

228 ROCKs also play a role in lymphocyte proliferation and migration.

229 ored, IFN-inducible protein that regulates T lymphocytes proliferation, differentiation, and developm

230 plication index (CCI), and the neutrophil-to-lymphocyte ratio (NLR) was used as an indicator of syste

231 il and lymphocyte frequencies and neutrophil/lymphocyte ratio after the allergen challenge.

232 dium, and pretransplant recipient neutrophil-lymphocyte ratio.

233 s, higher leukocyte counts and neutrophil-to-lymphocyte ratios.

234 TGF-beta, and IL-10) were tested on a mixed lymphocyte reaction between antigen-presenting cells and

235 In vitro mixed lymphocyte reactions revealed modulation of the recipien

236 ation in Mgl2(DTR) hosts activated cytotoxic lymphocytes, reduced Tregs, and inhibited metastasis dev

237 es, suggesting a robust adaptive cytotoxic T-lymphocyte response may, in part, confer resilience to S

238 We hypothesized that polarized T helper lymphocyte responses orchestrate progression of intrahep

239 massive transmural influx of leukocytes and lymphocytes, resulting in villous degeneration and lipid

240 7 with NS8593 or waixenicin A in wild-type B lymphocytes results in a significant decrease in SOCE, c

241 Comparing lymphocyte secretory profile from patients exhibiting hi

242 ng approach and analyzed individual CD8(+) T lymphocytes sequentially throughout the course of a vira

243 how that human and mouse tumour-infiltrating lymphocytes share a core tissue-residency gene-expressio

244 Patient's and father's lymphocytes showed reduced pSTAT4, nuclear translocation

245 A specific "peripheral lymphocyte signature" observed in patients with IgG4-RD,

246 otective IFN-gamma could be derived from any lymphocyte source and suppressed diabetogenic CD8(+) T-c

247 Our study provides significant insights into lymphocyte specificity during the recovery phase of EVD

248 ural killer T (iNKT) cells are innate-like T lymphocytes strongly implicated in tumor surveillance.

249 Lymphocyte subpopulations of 40 children and adolescents

250 cTFH cells and other lymphocyte subpopulations were characterized.

251 clusion, we show that SCARF-1 contributes to lymphocyte subset adhesion to primary human HSEC and cou

252 Circulating T-lymphocyte subset profiles in conventional HIV- BDD were

253 However, the T-lymphocyte subsets involved in the pathophysiology of hy

254 Treatments that increase GCR in these lymphocyte subsets may improve graft survival.

255 ts peaked around 1 year, whereas most memory lymphocyte subsets more gradually increased during the f

256 d us to investigate the ability of different lymphocyte subsets to produce this dichotomous eosinophi

257 In parallel, T lymphocyte subsets, as key constituents of the adaptive

258 TS were assessed for immunologic conditions, lymphocyte subsets, forkhead box P3 (FOXP3)(+) Treg cell

259 a), and expression of GCR were determined in lymphocytes subsets from cultured blood using flow cytom

260 racytoplasmic antigen 1-positive cytotoxic T lymphocytes, suggesting a robust adaptive cytotoxic T-ly

261 They arise from lymphocytes that are at various stages of development, a

262 Lymphomas represent clonal proliferations of lymphocytes that are broadly classified based upon their

263 ly, a substantial proportion of the adaptive lymphocytes that are found in the kidney displays a surf

264 he preimmune repertoire consists of mature T lymphocytes that have not yet been stimulated in the per

265 ectly investigate the antigen recognition of lymphocytes that mediate cancer regression in humans.

266 killer T cells (iNKT cells) are innate-like lymphocytes that protect against infection, autoimmune d

267 nt NKT (iNKT) cells are a subpopulation of T lymphocytes that recognize glycolipid antigens in the co

268 lta T cells are considered to be innate-like lymphocytes that respond rapidly to stress without clona

269 s of three-dimensional RI maps of individual lymphocytes, the morphological and biochemical propertie

270 site, where in synergy with tumor-redirected lymphocytes, they instructed TNFalpha expression, endoth

271 154 and stimulate the production of IgE by B lymphocytes through IL-25/IL-33 stimulation or TLR trigg

272 We isolated tumor-infiltrating lymphocytes (TIL) and intra-hepatic lymphocytes.

273 t studies have found that tumor-infiltrating lymphocytes (TIL) expressing PD-1 can recognize autologo

274 How tumor-infiltrating T lymphocytes (TILs) adapt to the metabolic constrains wit

275 g evidence indicates that tumor-infiltrating lymphocytes (TILs) are associated with clinical outcomes

276 antigen specificities of tumor-infiltrating lymphocytes (TILs) are not well understood.

277 ssociated with increased tumour infiltrating lymphocytes (TILs), however, MAPK activity is required f

278 n of T (CD3(+), CD4(+), CD8(+), and CD25(+)) lymphocytes, tissue macrophages, and dendritic cells (Ib

279 at can block T1D development by converting B lymphocytes to a disease-inhibitory CD73(+) regulatory s

280 stent immune activation causes impairment of lymphocytes to respond to chemotactic stimuli, thus prev

281 X induced immunogenic cell death and recruit lymphocytes to the tumor site.

282 an promote recruitment of tumor-infiltrating lymphocytes to the tumor, here we show that MEK inhibiti

283 rived from Epstein-Barr virus-immortalized B-lymphocytes to verify that the hyperexcitability of DG-l

284 of IL-12 and increased differentiation of T lymphocytes toward Th1 during infection.

285 novel outcome of S1P-mediated regulation of lymphocyte trafficking, whereby deletion of Spns2, eithe

286 val, and migration and is a key regulator of lymphocyte trafficking.

287 of the adaptive immune system, using CD4+ T-lymphocyte transcriptomics, would identify gene expressi

288 VE-cadherin expression and were required for lymphocyte transmigration.

289 iously unknown migratory behaviors of innate lymphocytes undergoing lineage differentiation revealed

290 naive CD8 T cells into effector cytotoxic T lymphocytes upon antigen stimulation is necessary for su

291 ues was shown to contain cells (macrophages, lymphocytes, vessel-associated cells) expressing sst2 on

292 Transmigration of purified lymphocytes was dependent on ADAM10 regulation of VE-cad

293 glia and infiltration of CD4(+) and CD8(+) T lymphocytes was observed.

294 The main effector lymphocytes were activated and displayed an early immune

295 s characterizing type 1, type 2, and type 17 lymphocytes were measured in sputum samples from 48 part

296 ractions with E-selectin than do circulating lymphocytes, which exhibit variable E-selectin binding a

297 encing of transcripts associated with memory lymphocytes, which highlights the power and necessity of

298 marker, we identified CD4-enriched, mature T lymphocytes with properties of T reg cells.

299 f lysosomes and Pxn at the contact zone of T lymphocytes with rE-cadherin-Fc-coated beads.

300 portance of analyzing metabolism in effector lymphocytes within in vivo inflammatory contexts and sug