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1 the hTNFR2 blocks the biological activity of lymphotoxin beta.
2 t CrmB and CrmD also inhibit the activity of lymphotoxin beta.
3 eron-gamma, tumor necrosis factor-alpha, and lymphotoxin-beta.
4 ive CD4 and CD8 T-cell subsets and decreased lymphotoxin-beta, a key factor for maintenance of FRC ne
5 s, which, in turn, removed a major source of lymphotoxin-beta, a survival factor for FRCs during SIV
6 (tumor necrosis factor alpha, IL-1beta, and lymphotoxin-beta), and leukocyte genes (S100A9, Aif1/Iba
7 on of lymphoid chemokines CXCL13, CCL19, and lymphotoxin-beta, and is associated with development of
8 anistically, we show that CD8(+) T cells and lymphotoxin beta are central mediators of HCC formation.
11 resembling that observed in B-cell-specific lymphotoxin-beta-deficient mice, including disruption of
13 AT5 regulates expression of the TNFalpha and lymphotoxin-beta genes in osmotically stressed T cells.
17 through the TNF receptor family member, the lymphotoxin-beta (LT-beta) receptor (LT-betaR), also reg
18 promoter regions, a CpG island in exon 4 of lymphotoxin beta (LTB), the 3' end of nuclear factor of
29 and cross-species consistent activation of a lymphotoxin beta/LTbetaR/RELB axis in hepatocarcinogenes
30 s and that this loss was caused by decreased lymphotoxin-beta mainly produced by the CD4 T cells.
31 dendritic cells (FDC) may act, we challenged lymphotoxin beta null and wild-type (wt) controls with a
32 tumor necrosis factor (TNF)-alpha, TNF-beta, lymphotoxin-beta, or TNFR1, TNFR2, Fas, or death recepto
33 eatment with interferon-gamma, which induced lymphotoxin beta receptor (LT beta R) expression, was re
34 implex virus entry mediator (HVEM) and LIGHT/lymphotoxin beta receptor (LT beta R) interactions decre
36 is study demonstrates enhanced expression of lymphotoxin beta receptor (Lt betaR) during the demyelin
37 Recent studies revealed that the lymphotoxin/lymphotoxin beta receptor (LT)/LTbetaR system activates
41 ediated by at least two receptors, including lymphotoxin beta receptor (LTbetaR) and herpes simplex v
42 cells including HT29 cells that express both lymphotoxin beta receptor (LTbetaR) and HVEM/TR2 recepto
43 tosis of various tumor cells expressing both lymphotoxin beta receptor (LTbetaR) and TR2/HVEM recepto
45 or receptors (TNFRs) as a homotrimer and via lymphotoxin beta receptor (LTbetaR) as a heterotrimeric
47 eady-state and after bone marrow transplant, lymphotoxin beta receptor (LTbetaR) controls entry of T
49 onditional gene-deficient mice, we find that lymphotoxin beta receptor (LTbetaR) directly controls th
52 (LT)alpha(1)beta(2) on inducer cells and the lymphotoxin beta receptor (LTbetaR) on stromal cells ini
53 dy sought to determine whether signaling via lymphotoxin beta receptor (LTbetaR) or herpesvirus entry
54 fusion protein between the IgG Fc domain and lymphotoxin beta receptor (LTbetaR) reduces lung fibrosi
57 tor (TNF) receptor superfamily members CD40, lymphotoxin beta receptor (LTbetaR), and B-cell-activati
58 bind the cytoplasmic domains of CD40 and the lymphotoxin beta receptor (LTbetaR), both of which are k
59 inflammation mediated by LIGHT, a ligand for lymphotoxin beta receptor (LTbetaR), not only stimulates
60 fic deletion of the thymus medulla regulator lymphotoxin beta receptor (LTbetaR), we show that thymic
61 a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration
69 nt region of IgG and extracellular domain of lymphotoxin beta receptor (LTbetaRIg) interrupted clonal
71 Induction of PNAd in mutant PPs requires lymphotoxin beta receptor activity, and its upregulation
72 f lymphotoxin was confirmed, as the use of a lymphotoxin beta receptor agonist results in partial res
73 both of its identified signaling receptors, lymphotoxin beta receptor and herpes virus entry mediato
74 rmation was dependent on lymphotoxin and the lymphotoxin beta receptor and independent of lymphocytes
75 LIGHT protected mice from colitis via the lymphotoxin beta receptor and was expressed mainly by my
76 y member 14 (TNFRSF14, also called HVEM) and lymphotoxin beta receptor are receptors for LIGHT that w
77 ion of LT and LIGHT signaling with a soluble lymphotoxin beta receptor decoy protein attenuated the d
79 xin axis, and pharmacological stimulation of lymphotoxin beta receptor might represent a novel therap
80 s, herpesvirus entry mediator on T cells and lymphotoxin beta receptor on stromal cells, are implicat
82 lary epithelial cells of mice lacking either lymphotoxin beta receptor or the lymphotoxin alpha-chain
83 ory distress, and shows that blockade of the lymphotoxin beta receptor pathway reverses the disease.
85 mphangiogenesis in the thyroid and implicate lymphotoxin beta receptor signaling in this process.
86 Notch-dependent Esam(hi) DC subset required lymphotoxin beta receptor signaling, proliferated in sit
87 found that an agonistic antibody against the lymphotoxin beta receptor was able to facilitate liver r
88 oid cells through interactions with LTbetaR (lymphotoxin beta receptor), without the requirement for
89 ts receptors, herpesvirus entry mediator and lymphotoxin beta receptor, are found in T cells and stro
90 , herpesvirus entry mediator (TNFRSF14), and lymphotoxin beta receptor, form an immune regulatory net
91 s receptors, herpes virus entry mediator and lymphotoxin beta receptor, it activates inflammatory res
92 e protein binds to the cytoplasmic domain of lymphotoxin beta receptor, which is a member of tumor ne
93 us-host disease model, Treg cells expressing lymphotoxin beta receptor-AIR, which can be activated by
94 tinal inflammation when transferred into the lymphotoxin beta receptor-deficient mice, and herpes vir
95 belonging to the TNF superfamily, by soluble lymphotoxin beta receptor-Ig (LTbetaR-Ig) inhibits the c
96 Blockade of LIGHT by its soluble receptors, lymphotoxin beta receptor-Ig or HVEM-Ig, inhibits the in
97 d state, blockade of this stimulation with a lymphotoxin beta receptor-immunoglobulin fusion protein
102 4 interacts with the cytosolic domain of the lymphotoxin-beta receptor (LT beta R) and weakly with th
103 Here we report that blocking LT alpha beta/lymphotoxin-beta receptor (LT beta R) interaction in viv
105 hese clones encode the cytoplasmic domain of lymphotoxin-beta receptor (LT betaR), which is a member
106 osis factor-alpha (TNF-alpha), whereas decoy lymphotoxin-beta receptor (LT-betaR) fusion protein had
107 nsduction of the TNF receptor 2 (TNFR2), the lymphotoxin-beta receptor (LT-betaR), CD40, CD30, and LM
108 ult mice was reduced by systemic blockade of lymphotoxin-beta receptor (LTbeta R) signaling with a so
109 re NIK for activation of NF-kappaB, only the lymphotoxin-beta receptor (LTbeta-R) is expressed in mel
113 ammatory mechanism, including membrane-bound lymphotoxin-beta receptor (LTbetaR) and CXC chemokine re
115 r, which binds two known cellular receptors, lymphotoxin-beta receptor (LTbetaR) and the herpesvirus
116 this effect through the interaction with the lymphotoxin-beta receptor (LTbetaR) but not herpes virus
118 Moreover, we show that signals through the lymphotoxin-beta receptor (LTbetaR) in DC are also requi
119 R4-activated canonical NF-kappaB pathway and lymphotoxin-beta receptor (LTbetaR) induced non-canonica
120 Here, we show that signaling through the lymphotoxin-beta receptor (LTbetaR) is critical for kidn
125 vation of innate immune effectors, STING and lymphotoxin-beta receptor (LTbetaR), results in CD8(+) T
126 equires innate lymphoid cells, which promote lymphotoxin-beta receptor (LTbetaR)-dependent maintenanc
130 In vitro, tumor necrosis factor (TNF) or lymphotoxin-beta receptor agonist can rescue expression
131 SF-14) is a ligand of stromal cell-expressed lymphotoxin-beta receptor and T cell-expressed herpes vi
132 of six single chain-Fv fragments of the anti-lymphotoxin-beta receptor antibody, statistically signif
135 de development during embryogenesis involves lymphotoxin-beta receptor engagement and subsequent diff
136 al-associated lymphoid tissue by LTbetaR-Ig (lymphotoxin-beta receptor human Ig fusion protein) treat
137 nobese diabetic (NOD) mice were treated with lymphotoxin-beta receptor immunoglobulin fusion protein
138 CICD was strongly activated by both TNF and lymphotoxin-beta receptor ligation in IKKbeta-/- MEFs an
139 as well as pharmacological inhibition of the lymphotoxin-beta receptor markedly delays tumor developm
143 nd on activated lymphocytes and binds to the lymphotoxin-beta receptor, which is generally present on
144 on in the thymi of lymphotoxin-deficient and lymphotoxin-beta receptor-deficient mice contributes to
145 lymphoplastic (aly/aly) or splenectomized B6 lymphotoxin-beta receptor-deficient mice demonstrated th
147 ions including BO, and that treatment with a lymphotoxin-beta receptor-immunoglobulin fusion protein
150 tion, BALB/c mice were treated in utero with lymphotoxin beta-receptor Ig fusion protein to generate
151 is factor superfamily member LIGHT activates lymphotoxin beta-receptor signaling, leading to the prod
152 activated, LTalphabeta(+), lymphocytes with lymphotoxin beta-receptor-expressing fibrosarcoma tumor
154 ated by intragraft TLOs and whether blocking lymphotoxin-beta-receptor (LTbetaR) signaling, a pathway
156 estingly, both the tumor necrosis factor and lymphotoxin beta receptors were down-regulated by NS5A.
159 tory cytokines, such as IL-1alpha, IL-1beta, lymphotoxin beta, TNFalpha, and IL-6, also increased.
160 colony-stimulating factor, stem cell factor, lymphotoxin beta, transforming growth factor beta1, and
161 eta (tumor necrosis factor/lymphotoxin-alpha/lymphotoxin-beta) triple knockout (KO) mice show a signi
164 kin (IL)-2, interferon-gamma (IFN-gamma) and lymphotoxin-beta, which mediate pro-inflammatory functio