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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
42 H chain (4F2 Ag, Slc3a2) was discovered as a lymphocyte-activation Ag.
43  previous observation in the requirement for lymphocyte activation and argue a revisit of the traditi
44 (k/k) protected Tlr7tg mice from spontaneous lymphocyte activation and autoantibody production.
45 olemic mice, increasing ApoA-I can attenuate lymphocyte activation and autoimmunity in SLE independen
46 g and cell death in preventing inappropriate lymphocyte activation and autoimmunity.
47  ubiquitin chain assembly complex (LUBAC) in lymphocyte activation and B-cell malignancy.1 These data
48 kin-4 (IL-4)-stimulated immune response of B-lymphocyte activation and cell proliferation.
49 ion, cellular ion homeostasis, leukocyte and lymphocyte activation and chemotaxis, protein transport,
50 ed processes, including cytokine production, lymphocyte activation and chemotaxis.
51 vels of Daf1 were correlated with markers of lymphocyte activation and cytokine production.
52 ulate not only lymphocyte apoptosis but also lymphocyte activation and development.
53 ntial role of this regulatory mechanism in T lymphocyte activation and effector function.
54 amily tyrosine kinases are key regulators of lymphocyte activation and effector function.
55           Ca(2+) is crucial for peripheral T-lymphocyte activation and effector functions, and influe
56  and ceramide homeostasis and participate in lymphocyte activation and eosinophil recruitment.
57 uiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive imm
58  and reorganization, which are essential for lymphocyte activation and function.
59 h differential progression and implicated in lymphocyte activation and function.
60 ype animals, coupled with significantly less lymphocyte activation and IFN-alpha production.
61  findings reveal a role for the LUBAC during lymphocyte activation and in B-cell malignancy.
62 chromatin modifications were compared during lymphocyte activation and in ES cells as well.
63 gand (FasL) can result in poor restraints on lymphocyte activation and in increased susceptibility to
64 ional factor that has an important role in T lymphocyte activation and inflammation.
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.
68                                              Lymphocyte activation and migration involve large-scale
69 t have redefined the role of ERM proteins in lymphocyte activation and migration.
70  contributes to the negative regulation of T-lymphocyte activation and peripheral tolerance.
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
73                     Ag recognition induces T lymphocyte activation and proliferation and acquisition
74 anscription factor NF-kappaB is required for lymphocyte activation and proliferation as well as the s
75                                            T lymphocyte activation and proliferation is involved in m
76 s, reflecting common changes associated with lymphocyte activation and proliferation.
77  The paracaspase MALT 1 is a major player in lymphocyte activation and proliferation.
78 ll functions, including antigen-stimulated T lymphocyte activation and proliferation.
79 ion of TCR signaling and preventing abnormal lymphocyte activation and proliferation.
80 a2+ (CRAC) channels, an essential signal for lymphocyte activation and proliferation.
81 riggers a cascade of events that result in T lymphocyte activation and promote positive and negative
82 apoptotic protease, has an essential role in lymphocyte activation and protective immunity.
83  of apoptotic bodies leading to dysregulated lymphocyte activation and signs of systemic autoimmunity
84 NFSF13) are important regulatory factors for lymphocyte activation and survival in mammals.
85  in their accumulation and, in turn, chronic lymphocyte activation and systemic autoimmune manifestat
86 lar location for protein expression during B lymphocyte activation and the DNA damage response.
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
89  protein expression as a function of human T lymphocyte activation and time.
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
94 ient mice had ameliorated disease, decreased lymphocyte activation, and decreased serum IgG.
95    These include antigen mimicry, polyclonal lymphocyte activation, and infection-mediated innate end
96  playing crucial roles in stem cell renewal, lymphocyte activation, and leukemogenesis.
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
103 ene expression during embryonic development, lymphocyte activation, and tumorigenesis.
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
106 munology is that metabolic reprogramming and lymphocyte activation are intricately linked.
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
112                                            T lymphocyte activation by antigen conditions adaptive imm
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
116                                            T-lymphocyte activation can be targeted by blocking co-sti
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
120                                 Furthermore, lymphocyte activation creates an environment favorable t
121                       2ME2 inhibits in vitro lymphocyte activation, cytokine production, and prolifer
122 c mechanisms, including microbe recognition, lymphocyte activation, cytokine signaling, and intestina
123                                            T lymphocyte activation decreased the requirement for pO(2
124                 Many patients with SCID have lymphocyte-activation defects that remain uncharacterize
125  late in infection, suggesting that there is lymphocyte activation despite substantial bystander apop
126 lupus pathology by broadly affecting T and B lymphocyte activation/differentiation.
127                                   Aberrant T lymphocyte activation due to signaling abnormalities, li
128           However, the role of C5a in innate lymphocyte activation during sepsis remains elusive.
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
131              As PD-L1 functions to fine tune lymphocyte activation, dysregulation of cytokines result
132                                              Lymphocyte activation following pristane injection was g
133  a highly specific event such antigen-driven lymphocyte activation, for example, polarization to a T
134              These cytokines are integral to lymphocyte activation, function, and proliferation.
135               Pharmacodynamic assessments of lymphocyte activation, function, proliferation and pheno
136  summarizes current experimental evidence of lymphocytes' activation, functional role, and crosstalk
137                      The inhibitory molecule lymphocyte activation gene 3 (LAG-3) and metalloprotease
138 fested by programmed cell death 1 (PD-1) and lymphocyte activation gene 3 (LAG-3) expression and a la
139                                              Lymphocyte activation gene 3 (LAG-3) is a CD4-related, a
140 o be involved in Treg modulation of DC, with lymphocyte activation gene 3 (LAG-3) playing a predomina
141          We show that aged mice deficient in lymphocyte activation gene 3 (LAG-3), an MHC class II bi
142 ltiple inhibitory receptors, including PD-1, lymphocyte activation gene 3 (LAG-3), T cell Ig mucin 3,
143 cells, such as programmed death 1 (PD-1) and lymphocyte activation gene 3 (LAG-3).
144 rkers programmed death receptor 1 (PD-1) and lymphocyte activation gene 3 (Lag-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
150      Despite expressing the cell surface Ags lymphocyte activation gene-3 (CD223) and CD103, neither
151                                              Lymphocyte activation gene-3 (LAG-3) is a CD4-related tr
152                                              Lymphocyte activation gene-3 (LAG-3) is a cell-surface m
153                                              Lymphocyte Activation Gene-3 (LAG-3) is a transmembrane
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
157                                              Lymphocyte activation gene-3 (LAG-3; CD223) is a CD4 hom
158                                              Lymphocyte activation gene-3 (LAG3) (CD223) is the third
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
162 e CD160, B- and T-lymphocyte attenuator, and lymphocyte activation gene-3 inhibitory pathways.
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
165 ed Programmed Death-1, CD160 and 2B4 but not lymphocyte activation gene-3.
166 immune regulation, including TGF-beta(3) and lymphocyte activation gene-3.
167 domain molecule of CD4 and the related gene, lymphocyte activation gene-3.
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 histone methyltransferase Ezh2 in regulating lymphocyte activation has been suggested, but the molecu
178 in response to TCR ligation, but its role in lymphocyte activation has not been addressed.
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
182          We also evaluated the kinetics of T-lymphocyte activation in both the systemic and the mucos
183                   A striking but transient T-lymphocyte activation in both the systemic and the mucos
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
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 ly significant and sensitive marker of early lymphocyte activation in vivo.
194 g complexes are dynamically regulated during lymphocyte activation in vivo.
195  lymphoma b (Cbl-b), a negative regulator of lymphocyte activation, in tumor-reactive CD8(+) T cells
196                                      Chronic lymphocyte activation is commonly present in the CNS of
197                                    Moreover, lymphocyte activation is impaired in C57BL/6 mice that e
198                                              Lymphocyte activation is initiated by a global increase
199                                           As lymphocyte activation is involved in the pathogenesis of
200 nisms, but their genome-wide regulation of T lymphocyte activation is largely unknown.
201                                              Lymphocyte activation is regulated by costimulatory and
202  down-regulation of CD62L that accompanies T lymphocyte activation is thought to redirect cells away
203 prolonged activation of IP(3)R1 required for lymphocyte activation is unclear.
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
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                                    Signaling lymphocyte activation molecule (SLAM) family receptors a
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
227                                The signaling lymphocyte activation molecule (SLAM)-associated protein
228        CD4(+) T cells deficient in signaling lymphocyte activation molecule (SLAM)-associated protein
229                                    Signaling lymphocyte activation molecule (SLAM)-associated protein
230 /SAP, an adaptor that recruits Fyn to signal lymphocyte activation molecule (SLAM)-related receptors.
231 is virus is the immune cell marker signaling lymphocyte activation molecule (SLAM).
232 e expressing the MV receptor human signaling lymphocyte activation molecule (SLAM, CD150) with human-
233                 BACKGROUND & AIMS: Signaling lymphocyte activation molecule (Slamf)1 is a co-stimulat
234 aired induction and maintenance of signaling lymphocyte activation molecule 6 expression, a TCR costi
235 induce PLZF, in part by regulating signaling lymphocyte activation molecule 6 expression.
236                                The signaling lymphocyte activation molecule F1 (SLAMF1) is both a mic
237 leukocyte immunoglobulin-like and signalling lymphocyte activation molecule families and a number of
238                                    Signaling lymphocyte activation molecule family (SLAMF)2/CD48 is a
239 inted to an important role for the signaling lymphocyte activation molecule family (slamf)6 surface r
240                CD84 belongs to the signaling lymphocyte activation molecule family of immunoreceptors
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
246                                    Signaling lymphocyte activation molecule-associated protein (SAP)
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
260                                    Signaling lymphocyte activation molecules (SLAMs) play an integral
261 d to evaluate the potential of platelets and lymphocytes activation molecules expression on the patho
262                                       Marked lymphocyte activation occurred immediately postinfection
263 aft rejection diseases, in which a sustained lymphocyte activation occurs in the presence of persiste
264 ed increased expression of CD69, a marker of lymphocyte activation, on diabetic T-cells.
265  siRNA-fusion protein complexes do not cause lymphocyte activation or induce IFN responses.
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
268               To identify new suppressors of lymphocyte activation, proliferation, and function, we e
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
271                                            T lymphocyte activation requires signal 1 from the TCR and
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
274       We have only recently begun to examine lymphocyte activation's relationship to adaptive immunit
275 tol 4,5-biphosphate (PIP2) is critical for T lymphocyte activation serving as a substrate for the gen
276       This was the only fraction to induce B-lymphocyte activation, since all the other fractions fai
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 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
282                               In particular, lymphocyte activation thresholds are subject to tuning,
283                      Selective inhibition of lymphocyte activation through abrogation of signal 3-cyt
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,
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                In metastatic LNs, signs of B lymphocyte activation were observed, as evidenced by 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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