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1 precursor) and lineage (B cell, T cell, and natural killer cell).
2 cells, helper T cells, effector B cells, and natural killer cells).
3 f cytotoxic lymphocytes (mostly T CD8(+) and natural killer cells).
4 he function and the activation status of the natural killer cell.
5 f total lymphocytes because of a decrease in natural killer cells.
6 presumably by regulatory T cells but also by natural killer cells.
7 ereby sensitizing melanoma cells to lysis by natural killer cells.
8 terations in CD4+ T cells, CD8+ T cells, and natural killer cells.
9 P) that is produced by cytotoxic T cells and natural killer cells.
10 also found to be less sensitive to purified natural killer cells.
11 ot required for the development of classical natural killer cells.
12 of local dendritic cells, and activation of natural killer cells.
13 us antiviral immune responses of T cells and natural killer cells.
14 cial role in the development and activity of natural killer cells.
15 olic granules of cytotoxic T lymphocytes and natural killer cells.
16 o lysis by both antigen-specific T cells and natural killer cells.
17 not dividing, fibroblasts to cytotoxicity by natural killer cells.
18 es that bound H1 hemagglutinin and activated natural killer cells.
19 cognition by antibody-dependent clearance by natural killer cells.
20 ll-free virus, and develop susceptibility to natural killer cells.
21 lls, notably monocytes, dendritic cells, and natural killer cells.
22 tein for monocytes/macrophages, T cells, and natural killer cells.
23 which in turn enhances tumor elimination by natural killer cells.
24 e receptor expressed on the surface of mouse natural killer cells.
25 jor forms of lymphomas arising from B, T, or natural killer cells.
26 hoblast defects, and a deficiency of uterine natural killer cells.
27 by clonal expansion of cytotoxic T cells or natural killer cells.
28 r the NKp30-activating receptor expressed on natural killer cells.
29 efficacy is dependent upon T cells, but not natural killer cells.
30 onse, which also involves CD8(+) T cells and natural killer cells.
31 lymphoproliferative disease of mature T and natural killer cells.
32 inflammatory signaling initiated by CD160 in natural killer cells.
33 ate immune cell functions of macrophages and natural killer cells.
34 ly expanded without affecting CD4+, CD8+, or natural killer cells.
35 peptide inhibits HLA-E-mediated cytolysis by natural killer cells.
36 capes of lymphomas that arise from B, T, and natural killer cells.
37 ntributions from CD5- splenocytes, including natural killer cells.
38 t alone was not able to stimulate T cells or natural killer cells.
39 he presence of T cells, dendritic cells, and natural killer cells.
40 umor-reactive cytotoxic T lymphocytes and/or natural killer cells.
41 sistance to the shear stress and attack from natural killer cells.
42 bers of monocytes, B cells, CD4 T cells, and natural killer cells.
43 ure T and B cells and jak3 in T and putative Natural Killer cells.
46 activation, IFNgamma response, CD16-mediated natural killer cell activation, and monocyte/macrophage
47 ytokine and chemokine levels, lymphocyte and natural killer cell activation, and viral antigen expres
48 lly, A5.1 ECs enhanced NKG2D interaction and natural killer cell activation, promoting NKG2D-dependen
51 munological defense, including inhibition of natural killer cell activity with ongoing lowering of Ig
52 nosuppression was an opportunity to discover natural killer cell alloreactions that eradicated acute
54 expression profiles of a receptor protein in natural killer cells among donors infected with human cy
56 ction, which results in increased peripheral natural killer cell and macrophage activities, elevated
57 their fusion machinery, leading to impaired natural killer cell and/or T lymphocyte degranulation an
58 y and adhesion molecule, expressed mainly by natural killer cells and CD8(+) T cells at steady state
60 Levels of serum IgM and IgA and circulating natural killer cells and class-switched memory B cells w
63 45 does reduce the viability of normal T and natural killer cells and decrease activated T-cell produ
64 T correlated with an increased proportion of natural killer cells and effector memory CD4(+) and CD8(
65 -cell subset frequencies, but an increase in natural killer cells and eosinophils occurred with IL-2
66 y clonal expansion of CD3+ T cells or CD3(-) natural killer cells and frequently is associated with a
69 eatment reduced this suppressive function of natural killer cells and increased survival of mice with
70 so in mice, mimics the cytotoxic activity of natural killer cells and increases the surface area avai
71 unodeficiency characterized by lack of T and natural killer cells and infant death from infection.
73 producers of IL-22 post-PH are conventional natural killer cells and innate lymphoid cells type 1.
75 inflammatory cytokine that stimulates T and natural killer cells and is critical for their survival
76 in MDA5(-/-) mice, but perforin induction by natural killer cells and levels of interferon gamma, int
77 OX in regulating development of CD4 T cells, natural killer cells and lymphoid tissue inducer cells,
78 s of innate lymphoid cells with conventional natural killer cells and lymphoid tissue inducer cells.
81 by complement deposition and accumulation of natural killer cells and monocytes/macrophages in capill
82 -bearing mice, and increased the activity of natural killer cells and of intratumoral-activated CD8(+
83 ng hepatic macrophages, T and B lymphocytes, natural killer cells and platelets, as well as key effec
84 eased IL-17 production by CD4(+) T cells and natural killer cells and recruited regulatory cells and
86 The NKG2D stimulatory receptor expressed by natural killer cells and T cell subsets recognizes cell
87 -H3 (CD276) is both an inhibitory ligand for natural killer cells and T cells and a tumor antigen tha
90 0-dependent elimination of dendritic cell by natural killer cells and that hydrocortisone improves ou
91 development of innate lymphocytes, including natural killer cells and the recently identified innate
93 g FcgammaRIIIa (expressed on macrophages and natural killer cells) and FcgammaRIIIb (expressed on neu
94 increased expression of IFNgamma-inducible, natural killer cell, and T cell transcripts, but less ex
95 , treatment-induced expansion of T cells and natural killer cells, and activation of interferon-gamma
99 e activation of dendritic cells, mast cells, natural killer cells, and CD8 T cells to mount an antitu
103 ype CD4 T cells, reduced T-bet expression by natural killer cells, and expansion of blood monocytes w
104 ed B cells to FcgammaR-expressing monocytes, natural killer cells, and granulocytes via trogocytosis.
105 ures tracking CD8 and CD4 T-cell activation, natural killer cells, and IFN activation associated sign
107 ting IFNgamma and Granzyme B CD4 T cells and natural killer cells, and lower number of FoxP3 regulato
109 e examine the roles of alveolar macrophages, natural killer cells, and neutrophils in antibody-mediat
110 The proliferation and production of B cells, natural killer cells, and plasmacytoid dendritic cells w
111 00R on macrophages, myeloid dendritic cells, natural killer cells, and T cells in SCC vs normal skin.
112 terized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced fre
122 were ineffective in ADCC assays with murine natural killer cells as effectors, whereas ADCP was equi
123 and discusses recent findings that identify natural killer cells as regulators of T cell function an
124 suppress the activation and cytotoxicity of natural killer cells as well as the activation, signalin
126 innate immune cells (antitumor macrophages, natural killer cells) associated with clearance of senes
128 itutive and alternate macrophage, B-cell and natural killer cell-associated transcripts (NKAT), indic
129 as immune checkpoint receptors in T cell and natural killer cell biology are just beginning to be unc
130 marily within antigen-experienced T cells or natural killer cells but less so in naive T or B cells.
131 s a distinct lineage from Th and circulating natural killer cells but shares circuitry devoted to fun
132 terestingly, tumor rejection did not involve natural killer cells but was associated instead with a m
133 The reduction of the interleukin-10 level in natural killer cells by hydrocortisone was partially dep
135 infiltrating Kupffer cells, mature activated natural killer cells (CD69+), and PD-1+ effector memory
136 ) IFN-gamma-producing group 1 ILCs (ILC1 and natural killer cells), CD8(+) cytotoxic T cells (TC1), a
137 Chronic lymphoproliferative disorders of natural killer cells (CLPD-NKs) and T-cell large granula
140 vealed only subtle changes in the T-cell and natural killer cell compartment, whereas B-cell differen
141 or the observed therapeutic effects and that natural killer cells constitute a critical human effecto
144 Compared with pretreatment levels, Treg and natural killer cell counts rose >fivefold (P < .001) and
145 hydrocortisone modulates the dendritic cell/natural killer cell cross talk in the context of posttra
146 effects of hydrocortisone on dendritic cell/natural killer cell cross talk were studied in a mouse m
147 IL-2 additionally promotes CD8(+) T cell and natural killer cell cytolytic activity and modulates T c
148 cancer cell growth, including stimulation of natural killer cell cytotoxic activity and repression of
149 elongation (RTEL1) mutation causing isolated natural killer cell deficiency and mutations in ras-asso
150 s corresponding and co-orchestrating B-cell, natural killer cell, dendritic cell, and innate lymphoid
155 ndent cell-mediated cytotoxicity produced by natural killer cells did not depend on AQP4 OAP assembly
157 The interaction of noncytotoxic decidual natural killer cells (dNK) and extravillous trophoblasts
158 DS1 (KIR2DS1) expressed by maternal decidual natural killer cells (dNK) and the presence of its ligan
159 s of HLA-G+ EVT with sample matched decidual natural killer cells (dNK), macrophages, and CD4+ and CD
160 d KLRG1 molecules) were increased in splenic natural killer cells during Pseudomonas aeruginosa infec
161 iated by interferon activated cells, such as natural killer cells, during the innate immune response.
163 16) report new mechanisms of human and mouse natural killer cell education by inhibitory and activati
169 ssed innate immune function, particularly of natural killer cells, from patients with unfavorable gen
172 veals that RAG endonuclease activity affects natural killer cell function, demonstrating that such do
176 tional T lymphocytes and T-regulatory cells, natural killer cells, gamma delta T cells, and other acc
177 ow that a network of diverse lymphoid cells (natural killer cells, gammadelta T cells, natural killer
178 FU treatment induced TSLP, HLA class II, and natural killer cell group 2D (NKG2D) ligand expression i
180 sfer of tumor-specific cytotoxic T cells and natural killer cells, have been clinically translated fo
181 of interferon-gamma (IFN-gamma) by activated natural killer cells, IL-34-Mphi and M-CSF-Mphi prevent
182 d novel associations between variants in the natural killer cell immune pathway and prematurity in th
185 Malignant cells express ligands for the natural killer cell immunoreceptor NKG2D, which sensitiz
187 CAR-engineered HSCs may produce myeloid and natural killer cells in addition to T cells expressing t
188 increased activity of cytotoxic T cells and natural killer cells in BKVN and viremia samples resembl
191 review, we discuss evidence for the role of natural killer cells in multiple sclerosis and experimen
192 to provide some understanding of the role of natural killer cells in regulating inflammation in the c
193 AT4 mediates IFNgamma release in T cells and natural killer cells in response to interleukin 12 (IL12
195 as designed to evaluate the possible role of natural killer cells in the reactivation of cytomegalovi
197 ased programmed death ligand 1 expression on natural killer cells (increased from 11.9% to 61.6%, P =
198 emorrhage-induced immunosuppression, splenic natural killer cells induced an interleukin-10-dependent
199 exDC-treated recipients showed a predominant natural killer cell infiltration and a presence of antib
200 ge in the balance of signals received by the natural killer cell influences its involvement in the en
201 Innate lymphocytes (gammadelta T cells, natural killer cells, innate lymphoid cells) are the maj
202 the utility of this microfluidic assay with natural killer cells interacting with tumor cells, and o
203 g., neutrophils, monocytes, macrophages, and natural killer cells) is followed by an adaptive immune
204 cted a study to ascertain the association of natural killer cell killer immunoglobulin-like receptors
206 s of immune cells including the conventional natural killer cells, lymphoid tissue inducers, type 1,
207 receptor 9 (TLR9), induces the activation of natural killer cells, macrophages, and antigen presentin
208 Here, I discuss how key immune cell types (natural killer cells, macrophages, dendritic cells, and
209 ting adenosine signaling is found to promote natural killer cell maturation and antitumor immunity an
210 nal data also indicate a function for HLA in natural killer cell-mediated innate immunity against HIV
211 -EMR1 IgG1 was evaluated in vitro by using a natural killer cell-mediated killing assay and in vivo i
212 type at diagnosis suggests CD8 T-cell and/or natural killer cell-mediated killing modulates humoral a
213 osylated anti-EMR1 mAb dramatically enhanced natural killer cell-mediated killing of eosinophils from
214 rate that mitophagy plays a critical role in natural killer cell memory formation following viral inf
215 ular mechanisms important to generate innate natural killer cell "memory" are poorly understood.
217 recruiting cytotoxic effector cells, such as natural killer cells, monocytes, and polymorphonuclear c
219 ations of T cells, B cells, dendritic cells, natural killer cells, myeloid-derived suppressor cells,
220 her organs, including innate lymphoid cells, natural killer cells, natural killer T cells, mucosal-as
221 atory hepatic macrophage infiltration, while natural killer cells, natural killer T cells, neutrophil
224 -2 abolish cytotoxic T lymphocytes (CTL) and natural killer cell (NK) cytotoxicity, and give rise to
229 ) T-cell ratio and increased CD16(+)CD56(hi) natural killer cells (NK), CD4(+) effector memory T cell
230 ident memory CD8(+) T cells (TRMs), resident natural killer cells (NKRs), and tumor-associated macrop
234 hostatic intolerance, salivary cortisol, and natural killer cell number and function were similar bet
237 PMVDS stimulated both cytotoxic T cells and natural killer cells of cell-mediated immunity to provid
240 nal lymphoproliferations arising from either natural killer cells or cytotoxic T lymphocytes (CTLs).
241 set of 13 unique genes, highly expressed in natural killer cells (p = 0.03), were significantly expr
244 we found that innate immune factors, such as natural killer cells, plasmacytoid dendritic cells, and
245 Because alterations of dendritic cells and natural killer cells play a central role in trauma-induc
248 Moreover, CD8+ T-cell, CD4+ T-cell and NK (natural killer) cell populations in splenocytes were ele
249 ction of IFN-gamma by lymphocytes, including natural killer cells, probably accounting for the enhanc
255 antigens and reduced ligation of activating natural killer-cell receptors may explain the loss of gr
256 peptide complexes probably affect T-cell and natural killer cell recognition, providing a sound basis
257 Immune recovery, including CD8(+) T-cell and natural killer cell reconstitution, was enhanced with bo
258 nsplantation, innate immune cells, including natural killer cells, recovered with virus rebound.
261 profile are due to a different proportion of natural killer cells responding in LUJV infection than t
262 might result from impaired CD8(+) T-cell and natural killer cell responses to EBV infection in these
263 pulmonary pathology, stronger and persistent natural killer cell responses, and the extended inductio
264 related to local and systemic recruitment of natural killer cells resulting in increased interferon-g
265 flammatory and regulatory cytokine profiles, natural killer cells showed a predominantly proinflammat
267 nduces the death of CD56(bright) NK cells, a natural killer cell subset whose expansion is correlated
268 ortion of CD4+ FoxP3+ T cells and CD56(high) natural killer cell subsets, which are cell subsets asso
270 eased Tregs without affecting CD4+, CD8+, or natural killer cells, suppressed inflammation, and great
271 ients have shown major shifts in circulating natural killer cells, T and B lymphocytes immediately af
272 roinflammatory cytokine responses by DCs and natural killer cells, Th1 development, phagocytic recept
275 are more probable to be recipients than B or natural killer cells; that trogocytosis occurs independe
276 ccumulating evidence for the contribution of natural killer cells, the key mediators of antibody-depe
277 t that TRAIL is part of the armamentarium of natural killer cells, these observations identify a new
279 RV144 vaccinee also inhibited the ability of natural killer cells to kill HIV-1-infected CD4(+) T cel
280 ng HGF-independent MET activity, and engaged natural killer cells to kill MET-expressing cancer cells
281 rated that anti-CD27 stimulated CD8(+) T and natural killer cells to release myeloid chemo-attractant
282 cytomegalovirus reactivation, the ability of natural killer cells to secrete interferon-gamma was sig
283 of tumoricidal effector cells, in particular natural killer cells, to the tumor stroma for antitumor
284 al immune cells, such as T helper type 1 and natural killer cells, to unleash neurotoxicity and infla
289 21R expression on CD8(+) T cells, but not on natural killer cells, was required for optimal anti-ErbB
290 major histocompatibility complex class I and natural killer cells were commonly downregulated in psor
292 the lungs, indicating that mice depleted of natural killer cells were much more susceptible to infec
298 trates of liver macrophages, neutrophils and natural killer cells, whereas hepatic CD4(+) T cells inc
299 roduction by IL-12p70-mediated activation of natural killer cells, whereas miR-146a and miR-146b over
300 (IFN-gamma) or TNF-alpha or cocultured with natural killer cells (which have been shown to induce an
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