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1 ed clusters of macrophages scattered between lymphocytes.
2 eceptor temporarily upregulated by activated lymphocytes.
3 (+) cell differentiation into CD56(+) innate lymphocytes.
4 trophils, and decreased progenitor cells and lymphocytes.
5 pecification programs of innate and adaptive lymphocytes.
6 eans to redirect the natural properties of T lymphocytes.
7 age trafficking when co-cultured with immune lymphocytes.
8 or activation and persistence of cytotoxic T lymphocytes.
9 et of gamma/delta T-cell receptor-expressing lymphocytes.
10 l blood, and elevated bronchoalveolar lavage lymphocytes.
11 globin, alkaline phosphatase, platelets, and lymphocytes.
12 as partial-body exposures produce fewer such lymphocytes.
13 ear factor of activated T-cells (NF-AT) in T-lymphocytes.
14 subtypes, dendritic cells, granulocytes, and lymphocytes.
15 ation with Epstein-Barr virus (EBV)-positive lymphocytes.
16 ed mechanical differences compared to normal lymphocytes.
17 s while promoting the development of B and T lymphocytes.
18 s well as increased populations of CD73(+) B lymphocytes.
19 n how Hivep3 impacts the maturation of these lymphocytes.
20 achieved 8.2 % gene recombination in mouse T lymphocytes.
21 d activation of antigen-specific cytotoxic T lymphocytes.
22 tinocytes, fibroblasts, dendritic cells, and lymphocytes.
23 in tumor-infiltrating, Fas receptor-positive lymphocytes.
24 umbers of CD4(+) T lymphocytes and CD20(+) B lymphocytes.
25 fic phenotype did not extend to other innate lymphocytes.
26  with their cognate receptors on cytotoxic T lymphocytes.
27 -CD40L interactions between DC1 and CD4(+) T lymphocytes.
28 o and in vitro contraction of activated CD8+ lymphocytes.
29 d cells actively engulf invading living Th17 lymphocytes, a process mediated by expression of activat
30 associated with clinical characteristics and lymphocyte aberrations.
31 ethod, we characterized the presence of anti-lymphocyte Abs in the whole cohort of 72 patients, as we
32 ciated invariant T (MAIT) cells are innate T lymphocytes activated by bacteria that produce vitamin B
33 , paradigm for lncRNA-mediated modulation of lymphocyte activation and signaling, with implications f
34 e production, and reduced expression of many lymphocyte activation genes.
35 philic immunoreceptor of the SLAM (signaling lymphocyte activation molecule) family-on either platele
36 cts gene expression in a manner dependent on lymphocyte activation status, contributing to the interi
37                            Infiltration of T lymphocytes, activation of microglia, and their interpla
38 sponse of patient-matched tumor infiltrating lymphocytes against antigens diferentially presented aft
39                             We characterized lymphocyte and monocyte populations as well as antigen-s
40 of antigen processing and presentation; more lymphocytes and associated cytokines; decreased extracel
41  T lymphocytes but fewer numbers of CD4(+) T lymphocytes and CD20(+) B lymphocytes.
42 intratumoral S100 dendritic cells, and CD8 T lymphocytes and CD57 natural killer cells in the ALNs(-)
43 proach to quantify MiHAs presented by B-cell lymphocytes and determined their expression levels by LC
44  human transcription factor TFIIH, in both B lymphocytes and epithelial cells, we hypothesized that S
45       Electron microscopy of patient-derived lymphocytes and fibroblasts from both patients with VPS1
46 examines interactions between group 2 innate lymphocytes and gastric microbes that enhance IgA produc
47 had significantly increased percentages of T lymphocytes and higher levels of a wide array of inflamm
48 ins (LMPs), is expressed in newly infected B lymphocytes and in post-transplant lymphomas.
49 agy, leading to the survival of autoreactive lymphocytes and increased autoantibody.
50            We visualized the interactions of lymphocytes and LVS-infected macrophages using confocal
51               Furthermore, there were higher lymphocytes and M1 macrophage infiltration in high mutat
52                       We show that apoptotic lymphocytes and macrophages release specific metabolites
53 he repression of multiple gene programs in B lymphocytes and maintains the adult B-2 cell fate.
54  between the T-cell receptor of CD4-positive lymphocytes and MHC II on antigen-presenting cells.
55 n conclusion, we identified that circulating lymphocytes and monocytes of individuals simultaneously
56 Significant increases were also apparent for lymphocytes and monocytes, accompanied by locally elevat
57 immune system and is secreted by cytotoxic T lymphocytes and natural killer cells to help eliminate v
58 th ligand 1 (PD-L1) microenvironment in live lymphocytes and selectively labeled within an immunosyna
59          Close proximity between cytotoxic T lymphocytes and tumour cells is required for effective i
60 dicated that CD20(+) B lymphocytes, CD8(+) T lymphocytes, and CD11c(+) cells are susceptible to IAV i
61 enic bacteria, remained nonimmunogenic for T lymphocytes, and increased bioavailability in tear fluid
62 r role in dictating the migratory pattern of lymphocytes, and thus vaccine efficacy in mucosal tissue
63 , respectively, within skin-homing/cutaneous lymphocyte antigen (CLA)(+) versus systemic/CLA(-) T cel
64 ell death 1 ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) immune checkpoints led to
65        Despite administration of cytotoxic T lymphocyte antigen 4 (CTLA-4) immunoglobulin (Ig), Qa-1
66 ge-specific effects of CTLA4-Ig (cytotoxic T-lymphocyte antigen 4-Ig), a fusion protein blocking cost
67 ndosome-localized thiolreductase (GILT), and lymphocyte antigen 6 family member E (LY6E), the three c
68                                              Lymphocyte antigen receptor repertoire deep sequencing d
69 rce of diverse immunoglobulin repertoires, B lymphocytes are an indispensable part of humoral immunit
70                             TIPE-deficient T lymphocytes are completely pilot-less: they are unable t
71                                            B lymphocytes are important players of the adaptive immune
72 embryogenesis and continuing even as matured lymphocytes are primed and educated in adult tissue.
73                                              Lymphocytes are some of the most motile cells of vertebr
74                                         Th17 lymphocytes are therefore critical for selective CNS ent
75 eptides derive from human proteins, to which lymphocytes are tolerant.
76 rs in the lamina propria and intraepithelial lymphocytes are unaffected.
77 sults from this study demonstrate that tumor lymphocytes, assessed by TCR repertoire quantification b
78  express the skin homing receptors cutaneous lymphocyte associated antigen and CCR4 (Ccr4), associate
79 mmed death ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) for cancer immu
80  cell death protein 1 (PD-1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4), which limit T
81  death ligand 1 (PD-1:PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4):B7-1 are among
82  2 received a combination of anticytotoxic T-lymphocyte-associated protein 4 and anti-PD-1 antibodies
83 o follow-up suggests a potential effect on T-lymphocytes at HLA-B(*)55:01.
84 e line is an ideal tool to study cytotoxic T lymphocyte biology and to optimize personalized immunoth
85 e review advances in understanding of innate lymphocyte biology with a focus on skin disease and the
86 pment and/or expansion of immune-suppressive lymphocytes (Bregs and Tregs).
87 quencies of CD19+CD24hiCD38hi transitional B lymphocytes (Bregs) increased from a median of 6% before
88 l mucosal monocytes/macrophages and CD8(+) T lymphocytes but fewer numbers of CD4(+) T lymphocytes an
89 he metabolic shift induced in human CD4(+) T lymphocytes by stimulation is characterized by an upregu
90                                              Lymphocyte CB(2)depletion also exacerbated JWH133 self-a
91 y infected biopsies indicated that CD20(+) B lymphocytes, CD8(+) T lymphocytes, and CD11c(+) cells ar
92 ining bronchoalveolar lavage (BAL) fluid for lymphocyte cellular analysis, and suggestions for transb
93 ions were made in favor of obtaining BAL for lymphocyte cellular analysis, transbronchial lung cryobi
94              Latest median donor myeloid and lymphocyte chimerism were 100% (range, 0-100) and 100% (
95 isplayed a significant decrease in hepatic B lymphocytes compared to untreated mice as assessed by hi
96                            Within FLAgs, the lymphocytes compartmentalize according to their chemokin
97                                              Lymphocyte conditioned media (CM) induced epithelial-mes
98 subset of TNBCs with high tumor-infiltrating lymphocyte content.
99  (N0 vs rest), number of tumour-infiltrating lymphocytes (continuous variable), subtype (HER2-enriche
100                                     Immune T lymphocytes control the replication of Francisella withi
101                                 Low absolute lymphocyte count (ALC) has potential to be a useful and
102 4] x 10(9) cells/L, p = 6.93 x 10(-57)), but lymphocyte count was less consistent (0.016 [0.007, 0.02
103 itive and potentially causal relationship of lymphocyte count with systolic BP and diastolic BP.
104 the curve >0.70), as were low albumin level, lymphocyte count, monocyte count, and ratio of periphera
105 2.1 ug/mL, P = .004) levels, and lower nadir lymphocyte counts (0.09 vs. 0.4 x 10(3) /uL, P = .006).
106 rbidities, more systemic symptoms and higher lymphocyte counts and C-reactive protein levels.
107 e 46 patients who died were older, had lower lymphocyte counts and estimated glomerular filtration ra
108  The lead SNP was also associated with lower lymphocyte counts and in silico follow-up suggests a pot
109 tics of temperature, C-reactive protein, and lymphocyte counts mirrored the remitting/relapsing SARS-
110 erum albumin and cholesterol concentrations, lymphocyte counts, age, body mass index (BMI), complicat
111 group significantly depended on infiltrating lymphocyte counts, with patients who showed both an earl
112 ients with an early hypoxia response but low lymphocyte counts.
113               These TMPs inhibit cytotoxic T lymphocyte (CTL) activity both in vitro and in vivo, and
114 modeling, and suppression of the cytotoxic T lymphocyte (CTL) response.
115 gnature, and the ratio of CD8(+) cytotoxic T lymphocytes (CTL) to CD68(+) macrophages both predict di
116 d infiltration and activation of cytotoxic T lymphocytes (CTLs) and CD103+ cross-presenting dendritic
117 lytic lymphocytes-including CD8+ cytotoxic T lymphocytes (CTLs) and natural killer cells-and regulate
118 ogical synapse formation between cytotoxic T lymphocytes (CTLs) and the target cells they aim to dest
119 n vivo molecular imaging of CD8+ cytotoxic T lymphocytes (CTLs) in response to anti-PD-L1 therapy.
120 teins also occurs from activated cytotoxic T lymphocytes (CTLs) where they have recently been reporte
121 lls to evade killing mediated by cytotoxic T lymphocytes (CTLs), we performed genome-wide CRISPR scre
122 ) expression to evade killing by cytotoxic T lymphocytes (CTLs).
123 resents a new model of peripherin-reactive B lymphocyte-dependent autoimmune neuritis.
124 ic HL (nodular sclerosis, mixed cellularity, lymphocyte-depleted or lymphocyte-rich HL), which accoun
125 ancreatitis, adrenocortical hyperplasia, and lymphocyte depletion of spleen and lymph nodes.
126 tious mononucleosis and cancers, including B lymphocyte-derived Burkitt lymphoma and immunocompromise
127 rized endocervical cells with HIV-1-infected lymphocyte-derived cells, we discovered endocervical+BVA
128            Besides, boldine reduced the Th17-lymphocyte detection and response and increased the Treg
129 etection and response and increased the Treg-lymphocyte detection and response in periodontitis-affec
130                                              Lymphocyte development is a complex and coordinated path
131 utations in the EOMES gene (12%) involved in lymphocyte development, PI3K-AKT/mTOR (6%), and loss-of-
132 ether antiviral response of peripheral blood lymphocytes differs between HG patients and healthy indi
133 ver, delivering large biologics to primary T lymphocytes directly in vivo is technically challenging
134                            Therefore, immune lymphocytes directly limit intracellular bacterial repli
135                    CD8(+) tumor-infiltrating lymphocytes displayed low expression of CD2 in the major
136 ntly, we found that peripheral monocytes and lymphocytes do not express substantial amounts of pro-in
137  lipoxin A(4) (LXA(4)) has emerging roles in lymphocyte-driven diseases.
138  that is linked to its latent infection of B lymphocytes, during which virus replication is not suppo
139 y mechanisms by which LXRalphabeta governs T lymphocyte education and illuminate LXRalphabeta's indis
140                                        The T lymphocyte, especially its capacity for antigen-directed
141     Additionally, SARS-CoV-2-specific memory lymphocytes exhibited characteristics associated with po
142 e of Wnt5A-depleted MDSC, tumor-infiltrating lymphocytes expressed decreased PD-1 and LAG3, suggestin
143              However, adult Ezh2-deficient B lymphocytes expressed Lin28b, which encodes an RNA-bindi
144 e main sources of Ca(2+) influx in mammalian lymphocytes following antigen receptor stimulation are C
145           Moreover, both CD4(+) and CD8(+) T lymphocytes from Mtb infected, metformin treated animals
146  factors, and outcomes of post-HCT AIC and B-lymphocyte function following rituximab.
147 act on the nuclear factor-kappaB pathway and lymphocyte function.
148 ding IL-17, and increased consumption of the lymphocyte growth factor IL-7 before motor onset of HD.
149  of LVS-infected macrophages with LVS-immune lymphocytes halted LVS replication and inhibited the spr
150                                            B lymphocytes have immunological functions beyond Ab produ
151                  Moreover, mice lacking Th17 lymphocytes have reduced BBB leakage, microglial activat
152 ripheral immune cells, such as monocytes and lymphocytes, have also been found to play an important r
153          The molecular mechanisms regulating lymphocyte homing into lymph nodes are only partly under
154 in vivo immune abnormalities consistent with lymphocyte hyperactivity.
155 diated inhibition of RXR Function, PI3K in B lymphocytes, iCOS-iCOSL in T helper cells, and the role
156  repair activities across thousands of human lymphocytes, identifying known and novel cell-type-speci
157 genitors, but these cells maintained their B lymphocyte identity.
158                     In a subset of patients, lymphocyte immunophenotyping, quantitative real-time PCR
159 ning was also observed in tumor-infiltrating lymphocytes in a subset of TNBCs with high tumor-infiltr
160  focused on understanding the role played by lymphocytes in autoimmune diseases of the central nervou
161 ents with COPD and monocytes/macrophages and lymphocytes in both patients with COPD and control subje
162  the phenotypes and HBV-specific response of lymphocytes in CHB patients stratified by serum HBsAg le
163 mpaired thymic development of PLZF(+) innate lymphocytes in germ-free (GF) neonatal mice is restored
164 eletion of the tumor suppressor TRAF3 from B lymphocytes in mice leads to the prolonged survival of m
165 esults suggest a substantial role for CD8(+) lymphocytes in suppressing the latency reversal effect o
166 ning demonstrated the presence of CD8+CD161+ lymphocytes in the arterial wall of two unruptured intra
167 , a large proportion of islet-infiltrating B lymphocytes in the NOD mouse model of T1D produce Abs di
168 vely correlated with the density of detected lymphocytes in tumor tissues, while expression of the ex
169 essential for antigen recognition by T and B lymphocytes in viral-host interaction.
170 ematopoietic cells was observed in cytolytic lymphocytes-including CD8+ cytotoxic T lymphocytes (CTLs
171 ociated with decreased IFNgamma response and lymphocyte infiltration in patient tumors.
172 owed both an early hypoxia response and high lymphocyte infiltration levels exhibiting significantly
173 ed with ISGs, CD4, CD8A, CD8B, and the tumor-lymphocyte infiltration phenotype.
174        Gene signature analysis confirmed the lymphocyte infiltration profile consistent with the hist
175 focal lymphocytes with moderate perivascular lymphocyte infiltration.
176 induces cell-cycle arrest in MF/SS malignant lymphocytes, inhibiting their proliferation but not thei
177 ment of innate (NK) and innate-like adaptive lymphocytes (iNKT, MAIT, and Vdelta2(+) gammadelta T cel
178  the exocrine glands become infiltrated with lymphocytes instigating severe damage to the salivary an
179 cal intracellular signaling molecule for T-B lymphocyte interactions, drives T follicular helper (Tfh
180 flammatory cells including neutrophils and T lymphocytes into the skin and hyperkeratosis/hyperplasia
181 oxygen and nutrients and recruit circulating lymphocytes into the SLO parenchyma, where they encounte
182 atments, and by adoptive transfer of treated lymphocytes into uninfected humanized mice.
183 , blood film microscopy to detect vacuolated lymphocytes is a rapid, readily accessible, and sensitiv
184                                Engineering T lymphocytes is an emerging approach in a variety of biom
185 k alleles, and drug-induced proliferation of lymphocytes isolated from patients support a role for th
186 kines release (cytokine storm) and loss of T lymphocytes (leukopenia) characterize the most aggressiv
187  functional hypoxia imaging and infiltrating lymphocyte levels as a potential predictor for treatment
188                                              Lymphocyte lineage specification and commitment requires
189 entional T cells, a heterogeneous class of T lymphocytes (MAIT, gammadeltaT, and iNKT cells) with pot
190                                         In T lymphocytes, MAL is found at the immunological synapse a
191 hoid organ that plays an essential role in T lymphocyte maturation and selection during development o
192                                   CD8+CD161+ lymphocytes may have an important role in the inflammato
193 achieved with immunotherapy that relies on T lymphocyte-mediated recognition of tumor antigens.
194                                              Lymphocyte migration is essential for adaptive immune su
195                 A subset of tumor-associated lymphocytes, most prominent in uveal melanoma, showed po
196 of chronic inflammatory cells, consisting of lymphocytes (n = 9), plasma cells (n = 6), and histiocyt
197 ings reveal novel functions of cullin 3 in B lymphocytes, namely regulating CD22 surface expression a
198 ecular pilot, akin to a ship's pilot, guides lymphocyte navigation, the nature of this pilot is unkno
199 a plasmacytoid dendritic cell-type I IFN-T/B lymphocyte network.
200 74% neutrophils [normal range, 40%-80%], 24% lymphocytes [normal range, 20%-40%], and 2% eosinophils
201                                   Developing lymphocytes of jawed vertebrates cleave and combine dist
202 report that mice deficient in conventional T lymphocytes or recombination-activating gene (Rag) faile
203  through hindering access to key epitopes by lymphocytes or through altering immune responses by bind
204 ological data on stromal tumour-infiltrating lymphocytes, PAM50 subtypes, and expression of 55 genes
205 ograms, and these cells acquired a fetal B-1 lymphocyte phenotype in vitro and in vivo.
206 8 HIV-negative MSM and 72 HIV-negative MSW T-lymphocyte phenotyping was performed 3 times biennially.
207                                            B lymphocytes play a central role in host immunity.
208                                            B lymphocytes play a critical role in adaptive immunity.
209 ies that highlight the important role that B lymphocytes play in cardiac and vascular disease.
210         Decidual NK cells (dNK) are the main lymphocyte population in early pregnancy decidual mucosa
211 killer T (iNKT) cells are a rare innate-like lymphocyte population that recognizes glycolipids presen
212 ng revealed reductions and rapid recovery in lymphocyte populations across lymphocyte subsets.
213    Mice developed expanded germinal center B lymphocyte populations as in other models of AID deficie
214 cy and provide preliminary insights into the lymphocyte populations that are key for the antiviral re
215  assess the clonal richness and diversity of lymphocyte populations; to track clone members over time
216 sical Hodgkin lymphoma, the disease-defining lymphocyte-predominant cells in NLPHL are consistently p
217 ccount for the majority of cases, or nodular lymphocyte-predominant HL.
218 nscription factors, specifically in murine B lymphocyte progenitors, but these cells maintained their
219 had significantly (p <= 0.05) increased CD4+ lymphocyte programmed death-1 and monocyte programmed de
220 creased neutrophils, accompanied by hampered lymphocyte proliferation but increased monocyte phagocyt
221                                              Lymphocyte proliferation was inhibited after 2 h of nora
222                           Low total helper T lymphocyte proportions and low naive helper T cell propo
223 ortant role for a myelin protein, myelin and lymphocyte protein (MAL), in the process of cell-to-cell
224 il to lymphocyte ratio (NLR) and monocyte to lymphocyte ratio (MLR) are respectively associated with
225                           High neutrophil to lymphocyte ratio (NLR) and monocyte to lymphocyte ratio
226 rognostic score (mGPS) and the neutrophil to lymphocyte ratio (NLR) and survival in patients with lun
227       In addition, the derived neutrophil-to-lymphocyte ratio and platelet count were significantly a
228 r level, neutrophil count, and neutrophil-to-lymphocyte ratio were all predictive of mortality (area
229 ory rate, white blood cell count, neutrophil/lymphocyte ratio, and lactate dehydrogenase level.
230 se (MELD) scores, AFP levels, and neutrophil-lymphocyte ratios (NLR); were more likely to have tumors
231 approaches, including peptide elution, mixed lymphocyte reaction, T-cell receptor (TCR) deep sequenci
232                        Reltecimod, a CD 28 T-lymphocyte receptor mimetic, inhibits T-cell stimulation
233 oligomerization domain-containing receptors, lymphocyte receptors, and cytokine receptors.
234 ngs reveal a role for vascular structures in lymphocyte recirculation through the spleen, indicating
235  cells during EAU resulting in alteration of lymphocyte repertoire by increasing levels of autoreacti
236 critical for central tolerance and diverse T-lymphocyte repertoire development, to provide lifelong d
237 d a TMP-specific H-2K(b)-restricted CD8(+) T lymphocyte response upon immunotherapy with cyclophospha
238  nodes induce activation of tumor-specific T-lymphocyte responses that can result in cytolytic target
239 a, and phosphorylated STAT3 as well as swift lymphocyte restoration.
240              Conditional deletion of Tph1 in lymphocytes resulted in selective impairment of ILC2(INF
241 s, mixed cellularity, lymphocyte-depleted or lymphocyte-rich HL), which account for the majority of c
242 e of the mesenteric adipose streaks contains lymphocyte-rich organoids comprised of a highly compacte
243                                    Antihuman lymphocyte serum (L1S1) antibody completely prevented ac
244 d progressively declined, whereas CD8+CD161+ lymphocytes significantly increased at days 5-9.
245 lymph node structures and therefore specific lymphocyte subpopulations.
246        However, they are the most abundant T-lymphocyte subset in some epithelial barriers such as mo
247          However, function of STAT3 in the B lymphocyte subset is not well understood.
248                          Absolute numbers of lymphocyte subsets and serum immunoglobulin levels were
249 id recovery in lymphocyte populations across lymphocyte subsets.
250 mbers over time, between tissues, and across lymphocyte subsets; to detect clonal expansion; and to d
251 thway are upregulated on tumour-infiltrating lymphocytes, suggesting that IL-18 therapy could enhance
252 ses breast cancer cells to evade cytotoxic T-lymphocyte surveillance, which leads to tumor growth.
253 n investigated in detail; CD4(+) cytotoxic T lymphocytes (suspected of promoting disease) and a speci
254 ears, with HIV viral load <50 copies/mL, and lymphocyte T-CD4 level >=200 cells/uL in the past 24 and
255                                  Cytotoxic T lymphocytes (T) and natural killer cells are the main cy
256 rates relies on the presence of B and T cell lymphocytes that aggregate in specific body sites to for
257  the context of cellular therapies may yield lymphocytes that are able to withstand harsh tumor metab
258 s several common pathways in MF/SS malignant lymphocytes that are associated with control of cell-cyc
259 s a cell surface receptor present on B and T lymphocytes that is universally and strongly expressed o
260 lta T cells (gammadeltaT17 cells) are innate lymphocytes that participate in type 3 immune responses
261 te lymphoid cells (ILCs) are tissue-resident lymphocytes that promote immunity to pathogens at mucosa
262 rease of dendritic cells and infiltration of lymphocytes throughout the pancreatic tumor compared to
263 bility to promote the continuous growth of B lymphocytes, thus providing significant new insight into
264 irect competition between tumor-infiltrating lymphocytes (TIL) and cancer cells for metabolic resourc
265 how that P2X7 activity in tumor-infiltrating lymphocytes (TIL) induces cellular senescence and limits
266 nvironment harboring more tumor infiltrating lymphocytes (TILs) and up-regulation of inflammatory sig
267  vivo-expanded autologous tumor-infiltrating lymphocytes (TILs) can mediate complete regression of ce
268 expansion and function of tumor-infiltrating lymphocytes (TILs) for treating cancer patients with ado
269  epitopes recognized by tumor-infiltrating T lymphocytes (TILs) from eight melanoma patients for all
270       The distribution of tumor-infiltrating lymphocytes (TILs) within the tumor microenvironment pro
271 (ACT) of ex vivo expanded tumor-infiltrating lymphocytes (TILs).
272 stochemical stainings for tumor-infiltrating lymphocytes, tissue-based hypoxia, and microvascular mar
273 t tumors induce de novo steroidogenesis in T lymphocytes to evade anti-tumor immunity.
274 ection and differentiation of the responding lymphocytes to generate a multitude of cell fates.
275 nly serves to amplify the number of specific lymphocytes to mount a robust protective response to the
276                                    For CD8 T lymphocytes to mount responses to cancer and virally-inf
277    Trafficking of alpha(4)beta(7)-expressing lymphocytes to the gut is mediated by MAdCAM, the natura
278 mph node addressin, and the extravasation of lymphocytes to the omental and mesenteric adipose tissue
279 hil interactions during migration on overall lymphocyte trafficking patterns in confined environments
280 erous genes, including genes encoding innate lymphocyte transcription factors, specifically in murine
281  lipidoids that are particularly potent in T lymphocytes transfection.
282                                 Regulatory T lymphocytes (Treg) play an important role in preventing
283 intervention induces functional regulatory T lymphocytes (Tregs) in mouse lung experimentally inflame
284                                     Dividing lymphocytes typically rely on aerobic glycolysis over ox
285 other NCRs that are expressed on activated T lymphocytes, V-type immunoglobulin domain-containing sup
286 ity of neutrophils to recirculate, much like lymphocytes via L-selectin and high endothelial venules
287                  Co-localization of B- and T-lymphocytes was observed.
288                                     Cultured lymphocytes were analyzed for cytokine secretion profile
289                 Subsequently, vaccine-primed lymphocytes were collected and reinfused after a standar
290                                        Blood lymphocytes were quantified by flow cytometry and antige
291  the evidence for clonal expansion in innate lymphocytes, which has primarily been observed in natura
292        Notably, transfection of the affected lymphocytes with MAGT1 mRNA restored both N-glycosylatio
293    Skin biopsy revealed acanthosis and focal lymphocytes with moderate perivascular lymphocyte infilt
294 tions, neutrons produce more heavily-damaged lymphocytes with multiple micronuclei/binucleated cell,
295 in vitro transduction of normal human CD4+ T lymphocytes with NPM-ALK results in their immortalizatio
296 atural killer T (iNKT) cells are innate-like lymphocytes with unique signaling requirements for their
297 ng the parallels between innate and adaptive lymphocytes, with a particular focus on NK cells and CD8
298  analysis of specific migratory behaviors of lymphocytes within the tissue microenvironment can provi
299 ural killer T (iNKT) cells are self-reactive lymphocytes, yet how this lineage attains self-tolerance
300  that sorting the most migratory cytotoxic T lymphocytes yields a pool of cells with enhanced cytotox

 
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