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1 group include the gamma-delta T cell and the Natural Killer T cell.
2 velopment of alphabeta T cells and invariant natural killer T cells.
3 n loss of conventional T cells and invariant natural killer T cells.
4 CD1d presents lipid antigens to natural killer T cells.
5 dual host T-cell subsets to favor regulatory natural killer T cells.
6 osis were conventional CD4+CD3+ T cells, not natural killer T cells.
7 II MHC-restricted CD4+ T cells but, rather, natural killer T cells.
8 ntified subgroup of T cells, CD1d-restricted natural killer T cells.
9 ds with high affinity to CD1d and stimulates natural killer T cells.
10 ncomitant to increased cytolytic activity of natural killer T cells.
11 velopment of B, alphabetaT, gammadeltaT, and natural killer T cells.
12 in knockout (beta2M-/-) mice lack CD8+ T and natural killer T cells.
13 nd natural killer cells but lack Valpha14(+) natural killer T cells.
14 to a specialized subset of T cells known as natural killer T cells.
15 e was independent of CTLs, natural killer or natural killer T cells.
16 with the innate immune system and invariant natural killer T cells.
17 s, which are the major endogenous ligands of natural killer T cells.
18 for mucosa-associated invariant T cells and natural killer T cells.
19 roduction of alphabeta T cells and invariant natural killer T cells.
20 sexual transmission of HIV and stimulator of natural killer T-cells.
21 s and presents IL-15 in trans to neighboring natural killer/T cells.
24 nnate T-CD4 T cells, together with invariant natural killer T cells and gammadelta T cells, receive s
25 l killer T cell apoptosis, depleting hepatic natural killer T cells and inducing proinflammatory cyto
26 g food allergy include the role of invariant natural killer T cells and influences of dietary compone
27 al other specialized T-cell lineages such as natural killer T cells and innate mucosal-associated inv
29 in numbers of microparticles from invariant natural killer T cells and macrophages/monocytes (CD14(+
31 een mostly confined to TCRs from innate-like natural killer T cells and mucosal-associated invariant
33 synthesis (P < 0.01), together with reduced natural killer T cells and raised interleukin (IL)-12 an
35 amma response of natural killer cells and of natural killer T cells and the Th1 polarization of antig
37 ability to effectively stimulate CD8 T cell, natural killer T cell, and natural killer cell immunity.
38 curring CD4+CD25+ Foxp3+ regulatory T cells, natural killer T cells, and approximately 25% of NK cell
39 rtant roles for conventional CD4(+) T cells, natural killer T cells, and CD4(+)CD25(+)FoxP3(+) Tregs
40 dependent on the presence of regulatory host natural killer T cells, and expression of CD1d on donor
41 s (natural killer cells, gammadelta T cells, natural killer T cells, and innate-like CD8+ T cells) ar
42 T-cell repertoire, near-to-absent invariant natural killer T cells, and severely diminished mucosal-
43 ltered residual host T cell subsets favoring natural killer T cells, and the low incidence of GVHD wa
44 lastic large cell; and 1 each had extranodal natural killer/T cell, angioimmunoblastic, and precursor
45 nsufficient norepinephrine increases hepatic natural killer T cell apoptosis, depleting hepatic natur
47 Gammadelta T lymphocytes and CD1d-restricted natural killer T cells are classified as innate T lympho
51 ouse models of allergic asthma indicate that natural killer T cells are required for the development
52 for the autoreactive recognition of CD1d by natural killer T cells, are indispensable for the bindin
53 tes, including both natural killer cells and natural killer T cells, are unusually abundant in the li
54 used CD1d-tetramers, antibodies specific for natural killer T cells, as well as reverse-transcriptase
55 volved in Th2 inflammation such as invariant natural killer T cells, basophils, and interleukin-9 are
56 protein (GFP), revealed CD4+ memory T cells, natural killer T cells, basophils, mast cells, and eosin
57 ghly expressed in activated human CD8(+) and natural killer T cells, both of which have been implicat
58 nal repressor NKAP is required for invariant natural killer T cell but not conventional T cell develo
59 cytotoxic lineage T cells and into invariant natural killer T cells but did not signal the differenti
61 nuclear cells before and after activation of natural killer T cells by ligand alpha-galactosylceramid
62 Stimulation of CD1d-restricted semiinvariant natural killer T cells by using the CD1d ligand alpha-ga
64 t of naturally occurring regulatory T cells, natural killer T cells, CD4(+) and CD8(+) T lymphocytes,
65 -specific Th2 cells did not require B cells, natural killer T cells, CD8(+) T cells, or IFNgamma.
66 are also deficient in natural killer cells, natural killer T cells, CD8+ T lymphocytes, and TCRgamma
68 Microparticles from CD14(+) and invariant natural killer T cells correlated with levels of alanine
70 njected 4 days before partial hepatectomy to natural killer T cells- deficient mice or to anti CD1d1-
74 re NKAP conditional knockout mice, invariant natural killer T cell development is blocked at the doub
75 due to a role of the SAP-Fyn interaction in natural killer T cell development through the ability of
76 se 3 causes a similar block in the invariant natural killer T cell development, indicating that NKAP
77 mice have defects in natural killer cell and natural killer T cell development, suggesting a role for
87 tically, PE DHC enhances EAE in mice lacking natural killer T cells, fails to enhance EAE in Toll-lik
89 -galactosyl ceramide (alpha-GalCer) to mouse natural killer T cells, formally demonstrating both the
91 hat development of colitis involves not only natural killer T-cell functions, but also requires IL-13
93 ve and qualitative defects in CD1-restricted natural killer T cells have been reported in several aut
94 as been 10 years since the first workshop on natural killer T cells helped to launch a growth phase f
96 articular, little is known about the role of natural killer T cells in alcohol-induced liver injury.
97 cidates the role of vitamin D and CD8(+) and natural killer T cells in asthma exacerbation in a genom
99 the current study is to explore the role of natural killer T cells in impaired liver regeneration.
100 association between the number of invariant natural killer T cells in the airway and disease severit
102 studies in mice indicating a requirement for natural killer T cells in the development of allergen-in
103 Alcohol consumption induces an increase of natural killer T cells in the liver and a high sensitivi
104 to assess the frequency and distribution of natural killer T cells in the lungs and in the circulati
105 ernatively activated hepatic macrophages and natural killer T cells, in the absence of obesity or ins
109 ylceramide (alphaGC) that activate invariant natural killer T cells (iNKT cells) are being developed
118 rinsic block in the development of invariant natural killer T cells (iNKT cells) at their earliest pr
119 ortant mechanisms of activation of invariant natural killer T cells (iNKT cells) by microbes: direct
127 n that interacted with innate-type invariant natural killer T cells (iNKT cells) to regulate B cell r
128 t also promoted the interaction of invariant natural killer T cells (iNKT cells) with those neutrophi
129 -GFP(+) cells, which encompass 70% invariant natural killer T cells (iNKT cells), have been found pri
132 riant T (iT) cell subsets, such as invariant natural killer T cells (iNKT) and mucosal-associated inv
134 but markedly decreased numbers of invariant natural killer T cells (iNKT) as defined by staining wit
136 requirements for invariant Valpha14-bearing natural killer T cells (iNKT) in the thymus are poorly u
137 (GVHD) are regulated via recipient invariant natural killer T-cell (iNKT) interleukin-4-driven expans
140 way, we have previously found that invariant natural killer T cells (iNKTs) are involved in CM allerg
141 CD1d-restricted Valpha24-Jalpha18-invariant natural killer T cells (iNKTs) are potentially important
143 sets, B cells, regulatory T cells, invariant natural killer T cells [iNKTs], NK cells, and dendritic
144 ltiple innate lymphocyte lineages, including natural killer T cell, innate lymphoid cell, mucosal-ass
146 It has been shown that the proportion of natural killer T cells is markedly elevated during liver
147 uing member of the innate immune system, the natural killer T cell, is activated during bacterial inf
148 sed on a subset of CD4+ T helper 1 cells and natural killer T cells, is involved in lymphocyte homing
149 sis including the Hut 78 T-cell leukemia, JY natural killer T-cell leukemia, Daudi B-cell lymphoma, H
150 ncy were enhanced by coadministration of the natural killer T-cell ligand 7DW8-5, which heightened th
159 aberrantly overexpressed in the majority of natural killer/T-cell lymphoma (NKTL), an aggressive lym
160 her incidence of AITL, extranodal nasal-type natural killer/T-cell lymphoma and NK-cell leukemia (ENK
161 ies, including acute lymphoblastic leukemia, natural killer/T-cell lymphoma, and acute myeloid leukem
162 s, as well as non-Hodgkin, Hodgkin and nasal natural killer/T-cell lymphomas, although all three TET
163 t commonly caused by Wegener granulomatosis, natural killer/T-cell lymphomas, cocaine abuse, or infec
164 s have provided evidence that T lymphocytes, natural killer T cells, mast cells, and B cells also ent
166 romoting the activation of T lymphocytes and natural killer T cells, maturation of DCs, secretion of
168 -like and T helper type 2-like properties of natural killer T cells may originate largely from differ
172 innate lymphoid cells, natural killer cells, natural killer T cells, mucosal-associated invariant T c
173 o differences in the percentages of T cells, natural killer T cells, natural killer (NK) cells, macro
175 ge infiltration, while natural killer cells, natural killer T cells, neutrophils and dendritic cells
177 family receptors can affect innate immunity [natural killer T cell (NKT) and gamma-delta T-cell recep
178 g in reduced expression of genes critical to natural killer T cell (NKT) and gammadelta T-cell differ
179 b(+)Ly6C(hi)Ly6G(-) cells also enhance liver natural killer T cell (NKT) death in an Fas-dependent ma
180 This glycolipid activates innate Valpha14(+) natural killer T cell (NKT) lymphocytes, which drive DC
181 to an impaired thymic selection of Valpha14 natural killer T cells (NKT cells) and a subsequent redu
182 e T cell antigen receptor (TCR) expressed by natural killer T cells (NKT cells) and the antigen-prese
183 (MHC) class I homolog CD1d are recognized by natural killer T cells (NKT cells) characterized by eith
184 (+) T cells (T regulatory cells [Tregs]) and natural killer T cells (NKT cells) each protect against
186 glycosphingolipids (GSLs) to activate type I natural killer T cells (NKT cells) has been known for 2
189 rpose of this study is to identify invariant natural killer T cells (NKT cells) in cellular infiltrat
196 relation with an IL-15-mediated increase of natural killer T-cells (NKT) and the up-regulation in li
197 f antigen-presenting cell CD1d with distinct natural killer T-cell ("NKT") populations can induce rap
200 IL-9 production from CD4(+) T cells, but not natural killer T cells or innate lymphoid cells, suggest
201 ediated by heat shock proteins, glycolipids, natural killer T cells, or dendritic cells in disease pa
202 vity, our results strongly suggest that CD4+ natural killer T cells play a prominent pathogenic role
203 airway hyperreactivity, we hypothesized that natural killer T cells play an important role in human a
206 ines, dendritic cells, and type 1 T cells or natural killer T cells potentially drives pathogenic inf
207 is paramount, which results in expansion of natural killer T cells producing IL-13 (and perhaps IL-5
208 suppressed expression of interferon gamma by natural killer T cells, promoting hepatocyte proliferati
209 ide and antibodies specific to the invariant natural killer T-cell receptor in samples of bronchoalve
211 xpression of messenger RNA for the invariant natural killer T-cell-receptor domains Valpha24 and Vbet
213 secreted following the ligation of invariant natural killer T cell receptors to sphingolipids (SLs).
217 TIM-1-expressing, but not TIM-1-deficient, natural killer T cells responded to apoptotic airway epi
218 suppression of protective CD4(+) T cells and natural killer T-cell responses against ehrlichiae.
219 ng indicates a role for TCR beta in defining natural killer T cell specificity, despite the more rest
220 ers effector properties resembling invariant natural killer T cells, such as copious production of cy
221 igen-presenting cell-mediated stimulation of natural killer T cells, supporting the idea that this me
222 reducing the activity of natural killer and natural killer T cells that normally contribute to tumor
223 dual host T cell subsets to favor regulatory natural killer T cells that suppress GVHD and prevent or
224 wing host T-cell subsets to favor regulatory natural killer T cells that suppress GvHD by polarizing
225 pattern-recognition receptor, conferring on natural killer T cells the ability to sense and respond
227 irecting the innate-like effector program of natural killer T-cell thymocytes, is prominently associa
228 analysis of the invariant T-cell receptor of natural killer T cells to assess the frequency and distr
229 naive, wild-type CD4(+) Th cells depleted of natural killer T cells to Lck(cre)IL-4Ralpha(-/lox) mice
231 hich liver gamma-delta T cells and invariant natural killer T cells were found to be involved in IL-1
232 oduced IFN-alpha, whereas natural killer and natural killer T cells were the main source of IFN-gamma
234 ages (ie, Kupffer cells), natural killer and natural killer T cells, which constitute the innate immu
237 LC3), and innate-like lymphocytes, including natural killer T cells, with an emphasis on the known re
238 ses mediated by IFN-gamma and CD4(+) Th1 and natural killer T cells, with lower IL-10 secretion by T
239 lavage, and sputum induction were invariant natural killer T cells, with no significant differences
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