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1 Semaphorin 7a (Sema 7a) participates in lymphocyte activation.
2 +) T lymphocytes and is downregulated upon T lymphocyte activation.
3 a transcriptional signature indicative of B lymphocyte activation.
4 s-presentation is sufficient for cytotoxic T lymphocyte activation.
5 ortant for proviral genome transcription and lymphocyte activation.
6 isruption of the NFAT pathway and subsequent lymphocyte activation.
7 stive protease, did not affect the induced B lymphocyte activation.
8 otein CARMA1 is required for the TCR-induced lymphocyte activation.
9 a) is a novel PKC that plays a key role in T lymphocyte activation.
10 ion (STAT) pathway and play pivotal roles in lymphocyte activation.
11 naling microclusters are a common feature of lymphocyte activation.
12 re chronic viral infections, and defective T-lymphocyte activation.
13 f Cdk5-p35 expression that is required for T lymphocyte activation.
14 nal transduction with an important role in T lymphocyte activation.
15 for AIDS progression than was viral load or lymphocyte activation.
16 erly modulate the function and the extent of lymphocyte activation.
17 the major coreceptor of HIV-1, costimulate T lymphocyte activation.
18 e cell migration to draining lymph nodes and lymphocyte activation.
19 ck on tumorous tissues via the H2O2-mediated lymphocyte activation.
20 ependent increases in soluble CD25 reflected lymphocyte activation.
21 C) is a novel PKC that plays a key role in T lymphocyte activation.
22 aining elevated cytosolic Ca2+ levels during lymphocyte activation.
23 ease-activated Ca2+ channels is required for lymphocyte activation.
24 eir central and peripheral tolerance or in T lymphocyte activation.
25 HIF1alphaI.1 is a negative regulator of lymphocyte activation.
26 tive data providing mechanistic insight into lymphocyte activation.
27 ess CD28, the key costimulatory molecule for lymphocyte activation.
28 cytokinesis, focal adhesion disassembly, and lymphocyte activation.
29 different apoptosis inhibitors often impairs lymphocyte activation.
30 and is a more potent negative regulator of T lymphocyte activation.
31 cytokines, suggesting a role for AIF-1 in T-lymphocyte activation.
32 ric particle carriers to cascade cytotoxic T lymphocyte activation.
33 bute to increased translation rates during T lymphocyte activation.
34 fic mAb suggests a role for Thy-1 in mouse T lymphocyte activation.
35 drugs may disrupt self-tolerance, leading to 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 re capable of diminishing IL-18-mediated CD4 lymphocyte activation.
40 ance of PKC localization for IS dynamics and lymphocyte activation.
41 ls, after their deamidation by TG2, induce T-lymphocyte activation accompanied by autoantibody produc
43 previous observation in the requirement for lymphocyte activation and argue a revisit of the traditi
45 olemic mice, increasing ApoA-I can attenuate lymphocyte activation and autoimmunity in SLE independen
47 ubiquitin chain assembly complex (LUBAC) in lymphocyte activation and B-cell malignancy.1 These data
49 ion, cellular ion homeostasis, leukocyte and lymphocyte activation and chemotaxis, protein transport,
57 uiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive imm
63 gand (FasL) can result in poor restraints on lymphocyte activation and in increased susceptibility to
65 SIV-infected animals increased expression of lymphocyte activation and inflammatory response-associat
66 RNA miR-155 has been shown to be involved in lymphocyte activation and is expressed in Epstein-Barr v
67 and within non-lymphocyte cells involved in lymphocyte activation and migration into the airways.
71 These associations highlight key roles for lymphocyte activation and prioritize specific cytokine p
72 l disease was ameliorated by (i) suppressing lymphocyte activation and proinflammatory cytokine produ
74 anscription factor NF-kappaB is required for lymphocyte activation and proliferation as well as the s
81 riggers a cascade of events that result in T lymphocyte activation and promote positive and negative
83 of apoptotic bodies leading to dysregulated lymphocyte activation and signs of systemic autoimmunity
85 in their accumulation and, in turn, chronic lymphocyte activation and systemic autoimmune manifestat
87 4) is required during an immune response for lymphocyte activation and the generation of immunoglobul
88 rom the plasma but, in addition, modulates T-lymphocyte activation and the inflammatory response by d
90 ed to cell proliferation in cluster 1 and to lymphocyte activation and unfolded protein responses in
91 l nervous system contributes to peripheral T-lymphocyte activation and vascular inflammation in this
92 sease as well as lymphadenopathy, polyclonal lymphocyte activation, and accelerated memory T cell for
93 iciency virus type 1 (HIV-1) reservoir size, lymphocyte activation, and CCR5 expression in 114 CCR5(D
95 These include antigen mimicry, polyclonal lymphocyte activation, and infection-mediated innate end
97 tration by monocyte-macrophages, decreased T lymphocyte activation, and reduced myocardial damage dur
98 n of Jurkat T-cell attachment, inhibition of lymphocyte activation, and release of inflammatory cytok
99 it is required for embryonic development, T-lymphocyte activation, and resistance to necrosis induce
100 d in inflammation, cytokine signaling, and T-lymphocyte activation, and suppression of genes involved
101 dogenous DC-HIL is a negative regulator of T lymphocyte activation, and that this native inhibitory f
102 reas S1P1 is downregulated during peripheral lymphocyte activation, and this is associated with reten
104 erated via modulation of CD11c+ APC-mediated lymphocyte activation, and was associated with a decreas
105 omprising a mutant mouse CD80 (CD80w88a) and lymphocyte activation antigen-3 was engineered to concur
107 on-induced suppression of cytotoxic CD8(+) T-lymphocyte activation as a tumour-promoting mechanism.
108 cSRS2 induced potent memory CD4+- and CD8+-T-lymphocyte activation, as indicated by proliferation and
109 K, two Tec kinases activated downstream of T-lymphocyte activation, both of which are up-regulated in
110 ay is critical for antigen receptor-mediated lymphocyte activation, but its function in cytokine sign
111 vement of immunoreceptor microclusters tunes lymphocyte activation, but the underlying mechanisms are
113 fect of PD-1 engagement and ICOS blockade on lymphocyte activation by in vitro T-cell proliferation a
114 indicate that the Lck SH3 domain controls T lymphocyte activation by regulating MAPK pathway inducti
115 , largely orchestrate memory CD8(+) T and NK lymphocytes activation by differentiating into interleuk
117 uring respiratory-virus infection, excessive lymphocyte activation can cause pathology both in acute
118 hat both massive lymphocytosis and excessive lymphocyte activation could contribute to massive cytoki
119 Both massive lymphocytosis and excessive lymphocyte activation could contribute to massive cytoki
122 c mechanisms, including microbe recognition, lymphocyte activation, cytokine signaling, and intestina
125 late in infection, suggesting that there is lymphocyte activation despite substantial bystander apop
129 tor signaling is required for normal B and T lymphocyte activation during the adaptive immune respons
130 ent is a highly regulated event required for lymphocyte activation during the adaptive immune respons
133 a highly specific event such antigen-driven lymphocyte activation, for example, polarization to a T
136 summarizes current experimental evidence of lymphocytes' activation, functional role, and crosstalk
138 fested by programmed cell death 1 (PD-1) and lymphocyte activation gene 3 (LAG-3) expression and a la
140 o be involved in Treg modulation of DC, with lymphocyte activation gene 3 (LAG-3) playing a predomina
142 ltiple inhibitory receptors, including PD-1, lymphocyte activation gene 3 (LAG-3), T cell Ig mucin 3,
145 was important to their induction of CD25(+) lymphocyte activation gene 3 (LAG3)(+), CD49b(-), forkhe
146 glucocorticoid-induced TNF receptor [GITR], lymphocyte activation gene 3 [LAG3]), TH1/TH2 cytokines,
147 ell markers (forkhead box protein 3 [FOXP3], lymphocyte activation gene 3 [LAG3], and glucocorticoid-
148 IL-10, inducible T-Cell costimulator (ICOS), lymphocyte activation gene 3 protein (LAG-3), and CD49b,
149 sion patterns for several markers, including lymphocyte activation gene 3, KLRG1, CD103, ICOS, CTLA-4
154 luating the benefits of systemic blockade of lymphocyte activation gene-3 (LAG-3) signals to improve
155 ytotoxic T-lymphocyte attenuator-4 (CTLA-4), lymphocyte activation gene-3 (LAG-3), and programmed dea
156 D-1), T cell immunoglobulin mucin-3 (TIM-3), lymphocyte activation gene-3 (LAG-3), cytotoxic T-lympho
159 tio, 8.7; confidence interval, 2.4-31.2) and lymphocyte activation gene-3 (odds ratio, 3.3; confidenc
160 xpress high levels of programmed death-1 and lymphocyte activation gene-3 and modestly suppress the p
161 Tregs were activated in vivo, and when using Lymphocyte Activation Gene-3 as a selection marker, as f
163 , including T-cell-related transcripts CD25, lymphocyte activation gene-3, Granzyme B, and interleuki
164 osts encode an additional CD4 family member, lymphocyte activation gene-3, which is a marker for acti
169 ed cell death 1 (PD-1; also known as CD279), lymphocyte-activation gene 3 (LAG-3; also known as CD223
171 re characterized by the presence of CD49b(+) lymphocyte-activation gene 3 (LAG3)(+) TR1 cells, antige
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
177 histone methyltransferase Ezh2 in regulating lymphocyte activation has been suggested, but the molecu
179 eutic potential of costimulatory signals for lymphocyte activation have spurred a large amount of wor
180 We observed that LTA potently suppressed T-lymphocyte activation in a Toll-like receptor 2-independ
181 und to play a surprisingly prominent role in lymphocyte activation in addition to its well-known role
184 ominent increase in viral loads and CD4(+) T lymphocyte activation in controllers than in progressors
185 latory T (Treg) cell expression, spontaneous lymphocyte activation in lymphoid organs was observed in
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
192 To assess the role of KCa3.1 channels in lymphocyte activation in vivo, we studied T cell functio
195 lymphoma b (Cbl-b), a negative regulator of lymphocyte activation, in tumor-reactive CD8(+) T cells
202 down-regulation of CD62L that accompanies T lymphocyte activation is thought to redirect cells away
204 signaling to NF-kappaB, essential for normal lymphocyte activation, is dysregulated in several types
205 sult in decreased antigen presentation and T-lymphocyte activation, leading to incomplete and/or weak
206 on, suggesting that apoptosis induction upon lymphocyte activation limits cellular and humoral immune
207 papillary cell RCC aberrantly expressing the lymphocyte activation marker CD70, a member of the tumor
208 tion led to a reduction in the expression of lymphocyte activation markers and resulted in reduced cy
209 ncreased expression of certain platelets and lymphocytes activation markers in chronic HCV and S. man
210 studies suggested that certain platelets and lymphocytes activation markers may have an impact on pro
211 espite unimpaired neutrophil recruitment and lymphocyte activation, mast cell-deficient mice have a d
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
216 cated immune cell receptors of the signaling lymphocyte activation molecule (SLAM) family during host
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
222 ive B and T cells interact via the signaling lymphocyte activation molecule (SLAM) family receptor, S
224 s (RNA-ICs), the expression of the signaling lymphocyte activation molecule (SLAM) family receptors C
225 -gamma-producing T cells expressed signaling lymphocyte activation molecule (SLAM), and SLAM activati
226 sed by the absence of a functional signaling lymphocyte activation molecule (SLAM)-associated protein
230 /SAP, an adaptor that recruits Fyn to signal lymphocyte activation molecule (SLAM)-related receptors.
232 e expressing the MV receptor human signaling lymphocyte activation molecule (SLAM, CD150) with human-
234 aired induction and maintenance of signaling lymphocyte activation molecule 6 expression, a TCR costi
237 leukocyte immunoglobulin-like and signalling lymphocyte activation molecule families and a number of
239 inted to an important role for the signaling lymphocyte activation molecule family (slamf)6 surface r
241 function of the mouse glycoprotein Signaling Lymphocyte Activation Molecule Family receptor (SLAMF) 4
242 le-positive thymocytes through the signaling lymphocyte activation molecule family receptor Ly108 mar
243 ters act as positive regulators of signaling lymphocyte activation molecule family receptor-specific
244 ind to phosphorylated tyrosines of signaling lymphocyte activation molecule family receptors in murin
245 KT cells and mediates signals from signaling lymphocyte activation molecule receptors that are exclus
247 d phagocytosis was independent of signalling lymphocyte activation molecule-associated protein (SAP)
248 er (PLZF) and the adaptor molecule signaling lymphocyte activation molecule-associated protein (SAP)
249 y a dysfunctional adapter protein, signaling lymphocyte activation molecule-associated protein (SAP),
250 utations in SH2D1A (Xq25) encoding signaling lymphocyte activation molecule-associated protein (SAP),
251 el, loss-of-function mutations in signalling lymphocyte activation molecule-associated protein (SAP,
252 s-linking, and relative paucity of signaling lymphocyte activation molecule-associated protein promot
253 ing lymphocyte activation molecule/signaling lymphocyte activation molecule-associated protein signal
254 nificant role in the regulation of signaling lymphocyte activation molecule-associated protein-mediat
255 cell development is controlled by signaling lymphocyte activation molecule/signaling lymphocyte acti
256 n molecules, CD84 and CD150 (SLAM [signaling lymphocyte activation molecule]), which are tyrosine pho
257 s were used to infect Vero or Vero/signaling lymphocyte-activation molecule (SLAM) cells in PRN assay
258 on is 2B4 (CD244), a member of the signaling lymphocyte-activation molecule (SLAM) family that binds
259 idence suggests a crucial role for signaling lymphocyte activation molecules (SLAMs) in the expressio
261 d to evaluate the potential of platelets and lymphocytes activation molecules expression on the patho
263 aft rejection diseases, in which a sustained lymphocyte activation occurs in the presence of persiste
266 line of CD4(+) T cells, a robust increase in lymphocyte activation, or change in the level of SIV-spe
267 (fl/fl)Cd4(Cre) mice resulted in spontaneous lymphocyte activation, primarily due to numerical and fu
269 s receptor indicate that IL-21 has a role in lymphocyte activation, proliferation, differentiation, a
270 MHC activation potency, suggesting that full lymphocyte activation required a minimal lifetime for TC
272 ed levels of corticosterone, which modulates lymphocyte activation responses and apoptosis during str
273 atment with Con A in a model of polyclonal T lymphocyte activation resulted in a greatly enhanced Th1
275 tol 4,5-biphosphate (PIP2) is critical for T lymphocyte activation serving as a substrate for the gen
279 ellular and molecular mechanisms following B lymphocyte activation that lead to IgM secretion are not
280 ough zeta-chain is critically important in T lymphocyte activation, the mechanism of the decreased ze
281 opathology, including nonspecific polyclonal lymphocyte activation, the need to test the direct impac
284 binding of the C3d fragment to Ag promotes B lymphocyte activation through coengagment of the BCR and
285 inia have the ability to directly suppress T lymphocyte activation through the virulence factor YopH,
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
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
297 ecause FDCs provide signaling that increases lymphocyte activation, we postulated that FDCs could inc
299 B7-DC and B7-H3 inhibit antigen-stimulated lymphocyte activation while B7-H2 serves in a regulatory
300 hanges in cellular metabolism that accompany lymphocyte activation, with a particular emphasis on glu
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