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4 ant role in antiviral immunity by regulating natural killer and CD8(+) T cells, epigenetic downregula
9 activation, IFNgamma response, CD16-mediated natural killer cell activation, and monocyte/macrophage
10 munological defense, including inhibition of natural killer cell activity with ongoing lowering of Ig
11 nosuppression was an opportunity to discover natural killer cell alloreactions that eradicated acute
13 as immune checkpoint receptors in T cell and natural killer cell biology are just beginning to be unc
14 elongation (RTEL1) mutation causing isolated natural killer cell deficiency and mutations in ras-asso
17 16) report new mechanisms of human and mouse natural killer cell education by inhibitory and activati
18 FU treatment induced TSLP, HLA class II, and natural killer cell group 2D (NKG2D) ligand expression i
19 ting adenosine signaling is found to promote natural killer cell maturation and antitumor immunity an
22 peptide complexes probably affect T-cell and natural killer cell recognition, providing a sound basis
23 pulmonary pathology, stronger and persistent natural killer cell responses, and the extended inductio
24 nduces the death of CD56(bright) NK cells, a natural killer cell subset whose expansion is correlated
27 increased expression of IFNgamma-inducible, natural killer cell, and T cell transcripts, but less ex
30 infiltrating Kupffer cells, mature activated natural killer cells (CD69+), and PD-1+ effector memory
33 ) T-cell ratio and increased CD16(+)CD56(hi) natural killer cells (NK), CD4(+) effector memory T cell
34 ident memory CD8(+) T cells (TRMs), resident natural killer cells (NKRs), and tumor-associated macrop
36 expression profiles of a receptor protein in natural killer cells among donors infected with human cy
39 unodeficiency characterized by lack of T and natural killer cells and infant death from infection.
40 producers of IL-22 post-PH are conventional natural killer cells and innate lymphoid cells type 1.
42 by complement deposition and accumulation of natural killer cells and monocytes/macrophages in capill
51 the utility of this microfluidic assay with natural killer cells interacting with tumor cells, and o
52 PMVDS stimulated both cytotoxic T cells and natural killer cells of cell-mediated immunity to provid
56 rated that anti-CD27 stimulated CD8(+) T and natural killer cells to release myeloid chemo-attractant
57 major histocompatibility complex class I and natural killer cells were commonly downregulated in psor
59 g FcgammaRIIIa (expressed on macrophages and natural killer cells) and FcgammaRIIIb (expressed on neu
60 innate immune cells (antitumor macrophages, natural killer cells) associated with clearance of senes
64 ype CD4 T cells, reduced T-bet expression by natural killer cells, and expansion of blood monocytes w
65 ures tracking CD8 and CD4 T-cell activation, natural killer cells, and IFN activation associated sign
67 e examine the roles of alveolar macrophages, natural killer cells, and neutrophils in antibody-mediat
68 s of immune cells including the conventional natural killer cells, lymphoid tissue inducers, type 1,
69 recruiting cytotoxic effector cells, such as natural killer cells, monocytes, and polymorphonuclear c
70 her organs, including innate lymphoid cells, natural killer cells, natural killer T cells, mucosal-as
71 atory hepatic macrophage infiltration, while natural killer cells, natural killer T cells, neutrophil
72 roinflammatory cytokine responses by DCs and natural killer cells, Th1 development, phagocytic recept
73 al immune cells, such as T helper type 1 and natural killer cells, to unleash neurotoxicity and infla
74 21R expression on CD8(+) T cells, but not on natural killer cells, was required for optimal anti-ErbB
85 kely resulted from expansion of a transduced natural killer clone in response to chronic Epstein-Barr
92 ata as the basis for the prognostic index of natural killer lymphoma (PINK), in which patients are st
97 activating receptor expressed on subsets of natural killer (NK) and T cells, interacts with its liga
98 as a major determinant of antibody-mediated natural killer (NK) cell activation in HT biopsies; howe
99 e requirement of type I interferon (IFN) for natural killer (NK) cell activation in response to viral
112 (MHC) Ib molecule Qa-1 impairs CD8 Treg and natural killer (NK) cell function and promotes a lupus-l
114 ssociated with certain HLA alleles and their natural killer (NK) cell immunoglobulin-like receptor (K
115 a HER2-dependent manner, reduced binding by natural killer (NK) cell inhibitory sialic acid-binding
117 (CMV-Tc), CD4+ (CMV-Th) T cell activity, and natural killer (NK) cell number were measured by flow cy
125 eness of anti-PD-L1/PD-1 agents in enhancing natural killer (NK) cell's function remains largely unkn
127 h anti-GD2 monoclonal antibody (mAb) directs natural killer (NK) cell-mediated antibody-dependent cel
130 o enhanced the recruitment and activation of natural killer (NK) cells and cytotoxic CD8(+) T cells t
131 ve and functional defects of innate effector natural killer (NK) cells and cytotoxic T-lymphocyte res
132 ptor NKp44, encoded by NCR2 and expressed on natural killer (NK) cells and innate lymphoid cells, rec
133 In this study, we evaluated the impact of natural killer (NK) cells and myeloid (mDCs) and plasmac
135 sufficient development and function of human natural killer (NK) cells and T cell subsets limit the a
136 tive T cells, but whether and how it affects natural killer (NK) cells and their alloreactivity is la
153 Human cytomegalovirus (CMV)-induced adaptive natural killer (NK) cells display distinct phenotypic an
154 bjected to middle cerebral artery occlusion, natural killer (NK) cells display remarkably distinct te
159 ing subsequent recruitment of hypercytotoxic natural killer (NK) cells expressing the CXCL16 receptor
165 cells and produce proinflammatory cytokines, natural killer (NK) cells have long been of clinical int
166 eral studies have evaluated the functions of natural killer (NK) cells in experimental animal models
168 s study, we examined a hypothesized role for natural killer (NK) cells in impacting disease progressi
169 trast to the extensive knowledge about human natural killer (NK) cells in peripheral blood, relativel
170 regulate metastasis, discuss the key role of natural killer (NK) cells in the control of metastatic d
171 ls and the percentage of active CD8(+) T and natural killer (NK) cells in the tumor microenvironment,
173 established, its role on the infiltration of natural killer (NK) cells into tumors remains unknown.
174 sh type 1 innate lymphoid cells (ILC1s) from natural killer (NK) cells is a gene signature indicative
189 ler cells engagers (BiKEs) which can bind to natural killer (NK) cells through the activating recepto
190 tly to antibody-mediated protection in vivo, natural killer (NK) cells were dispensable for protectiv
191 idled activation of cytotoxic T lymphocytes, natural killer (NK) cells, and macrophages resulting in
192 86 expression on peripheral blood monocytes, natural killer (NK) cells, and NK T cells was measured,
193 to generate all known ILC subsets, including natural killer (NK) cells, but not other leukocyte popul
194 c ligand of the activating NKG2D receptor on natural killer (NK) cells, gammadelta-T cells, and NKT c
195 pattern recognition receptors in myeloid and natural killer (NK) cells, has been shown to play both a
196 t patients and retain potential for EOMES(+) natural killer (NK) cells, interferon gamma-positive (IF
197 , however they also inhibit the functions of natural killer (NK) cells, key effectors of the Graft ve
198 several pro-allergic immune cells including natural killer (NK) cells, NKT cells, and memory CD8(+)
199 on of CD7 is largely confined to T cells and natural killer (NK) cells, reducing the risk of off-targ
200 ation, migration, and cytokine production in natural killer (NK) cells, suggesting that surface compo
202 analyses to define a STAT5 gene signature in natural killer (NK) cells, the prototypical ILC subset,
203 immune-mediated cell killing by T cells and natural killer (NK) cells, thereby suppressing metastati
205 ls, but less is known about their effects on natural killer (NK) cells, which help control metastasis
206 suggested a central role for neutrophils and Natural Killer (NK) cells, with underexpression of T- an
207 nalling only on NKG2D-bearing cells, such as natural killer (NK) cells, without broadly activating IL
230 e characterized plasmacytoid dendritic cell, natural killer (NK), and T-cell activation using flow cy
231 s showed that genes known to be expressed by natural killer (NK), lymphoid tissue inducer (LTi), and
234 antly induced both autologous and allogeneic natural killer (NK)-cell degranulation and NK-cell-media
235 T) cures the T-lymphocyte, B-lymphocyte, and natural killer (NK)-cell differentiation defect in inter
236 hocytes (IELs) lacking classical B-, T-, and natural killer (NK)-cell lineage markers (Lin(-)IELs) in
238 activating receptors that are engaged during natural killer (NK)-target cell contact remains undefine
239 (two clusters), serpins, cathepsins, and the natural killer (NK)/C-type lectin (CLEC) complex [6-12].
240 pressed genes, particularly those related to natural killer (NK)/CD8+ T-cell cytotoxicity, separated
247 (2017) reveal a critical role for invariant natural killer T (iNKT) cells in switching inflammation
251 ors (TCRs) drive the activation of invariant natural killer T (iNKT) cells, a specialized subset of i
254 by unfractionated conventional T, invariant natural killer T (iNKT) or gammadelta T cells, and is ch
258 und a potential association between absolute natural killer T (NKT) cell numbers and the subsequent d
259 the anti-influenza efficacy of the invariant natural killer T (NKT) cell superagonist, alpha-galactos
264 d with strongly reduced numbers of invariant natural killer T and regulatory T (Treg) cells and alter
265 associated with reduced numbers of invariant natural killer T and Treg cells that likely contribute t
266 g in reduced expression of genes critical to natural killer T cell (NKT) and gammadelta T-cell differ
267 ltiple innate lymphocyte lineages, including natural killer T cell, innate lymphoid cell, mucosal-ass
270 n that interacted with innate-type invariant natural killer T cells (iNKT cells) to regulate B cell r
272 way, we have previously found that invariant natural killer T cells (iNKTs) are involved in CM allerg
274 e T cell antigen receptor (TCR) expressed by natural killer T cells (NKT cells) and the antigen-prese
278 sets, B cells, regulatory T cells, invariant natural killer T cells [iNKTs], NK cells, and dendritic
282 the current study is to explore the role of natural killer T cells in impaired liver regeneration.
283 It has been shown that the proportion of natural killer T cells is markedly elevated during liver
285 innate lymphoid cells, natural killer cells, natural killer T cells, mucosal-associated invariant T c
286 ge infiltration, while natural killer cells, natural killer T cells, neutrophils and dendritic cells
287 njected 4 days before partial hepatectomy to natural killer T cells- deficient mice or to anti CD1d1-
291 (GVHD) are regulated via recipient invariant natural killer T-cell (iNKT) interleukin-4-driven expans
297 her incidence of AITL, extranodal nasal-type natural killer/T-cell lymphoma and NK-cell leukemia (ENK
298 ies, including acute lymphoblastic leukemia, natural killer/T-cell lymphoma, and acute myeloid leukem
299 s, as well as non-Hodgkin, Hodgkin and nasal natural killer/T-cell lymphomas, although all three TET
300 bitory receptor-mediated role for unlicensed natural killer (U-NK) cells in allogeneic graft facilita
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