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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
28 s and that this loss was caused by decreased lymphotoxin-beta mainly produced by the CD4 T cells.
29 dendritic cells (FDC) may act, we challenged lymphotoxin beta null and wild-type (wt) controls with a
30 tumor necrosis factor (TNF)-alpha, TNF-beta, lymphotoxin-beta, or TNFR1, TNFR2, Fas, or death recepto
31 eatment with interferon-gamma, which induced lymphotoxin beta receptor (LT beta R) expression, was re
32 implex virus entry mediator (HVEM) and LIGHT/lymphotoxin beta receptor (LT beta R) interactions decre
34 is study demonstrates enhanced expression of lymphotoxin beta receptor (Lt betaR) during the demyelin
35 Recent studies revealed that the lymphotoxin/lymphotoxin beta receptor (LT)/LTbetaR system activates
38 ediated by at least two receptors, including lymphotoxin beta receptor (LTbetaR) and herpes simplex v
39 cells including HT29 cells that express both lymphotoxin beta receptor (LTbetaR) and HVEM/TR2 recepto
40 tosis of various tumor cells expressing both lymphotoxin beta receptor (LTbetaR) and TR2/HVEM recepto
41 or receptors (TNFRs) as a homotrimer and via lymphotoxin beta receptor (LTbetaR) as a heterotrimeric
43 eady-state and after bone marrow transplant, lymphotoxin beta receptor (LTbetaR) controls entry of T
45 onditional gene-deficient mice, we find that lymphotoxin beta receptor (LTbetaR) directly controls th
48 (LT)alpha(1)beta(2) on inducer cells and the lymphotoxin beta receptor (LTbetaR) on stromal cells ini
49 fusion protein between the IgG Fc domain and lymphotoxin beta receptor (LTbetaR) reduces lung fibrosi
50 bind the cytoplasmic domains of CD40 and the lymphotoxin beta receptor (LTbetaR), both of which are k
51 inflammation mediated by LIGHT, a ligand for lymphotoxin beta receptor (LTbetaR), not only stimulates
52 fic deletion of the thymus medulla regulator lymphotoxin beta receptor (LTbetaR), we show that thymic
53 a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration
59 nt region of IgG and extracellular domain of lymphotoxin beta receptor (LTbetaRIg) interrupted clonal
61 Induction of PNAd in mutant PPs requires lymphotoxin beta receptor activity, and its upregulation
62 f lymphotoxin was confirmed, as the use of a lymphotoxin beta receptor agonist results in partial res
63 both of its identified signaling receptors, lymphotoxin beta receptor and herpes virus entry mediato
64 rmation was dependent on lymphotoxin and the lymphotoxin beta receptor and independent of lymphocytes
65 LIGHT protected mice from colitis via the lymphotoxin beta receptor and was expressed mainly by my
66 ion of LT and LIGHT signaling with a soluble lymphotoxin beta receptor decoy protein attenuated the d
68 xin axis, and pharmacological stimulation of lymphotoxin beta receptor might represent a novel therap
69 s, herpesvirus entry mediator on T cells and lymphotoxin beta receptor on stromal cells, are implicat
71 lary epithelial cells of mice lacking either lymphotoxin beta receptor or the lymphotoxin alpha-chain
72 ory distress, and shows that blockade of the lymphotoxin beta receptor pathway reverses the disease.
73 mphangiogenesis in the thyroid and implicate lymphotoxin beta receptor signaling in this process.
74 Notch-dependent Esam(hi) DC subset required lymphotoxin beta receptor signaling, proliferated in sit
75 found that an agonistic antibody against the lymphotoxin beta receptor was able to facilitate liver r
76 ts receptors, herpesvirus entry mediator and lymphotoxin beta receptor, are found in T cells and stro
77 e protein binds to the cytoplasmic domain of lymphotoxin beta receptor, which is a member of tumor ne
78 tinal inflammation when transferred into the lymphotoxin beta receptor-deficient mice, and herpes vir
79 belonging to the TNF superfamily, by soluble lymphotoxin beta receptor-Ig (LTbetaR-Ig) inhibits the c
80 Blockade of LIGHT by its soluble receptors, lymphotoxin beta receptor-Ig or HVEM-Ig, inhibits the in
81 d state, blockade of this stimulation with a lymphotoxin beta receptor-immunoglobulin fusion protein
85 4 interacts with the cytosolic domain of the lymphotoxin-beta receptor (LT beta R) and weakly with th
86 Here we report that blocking LT alpha beta/lymphotoxin-beta receptor (LT beta R) interaction in viv
88 hese clones encode the cytoplasmic domain of lymphotoxin-beta receptor (LT betaR), which is a member
89 osis factor-alpha (TNF-alpha), whereas decoy lymphotoxin-beta receptor (LT-betaR) fusion protein had
90 nsduction of the TNF receptor 2 (TNFR2), the lymphotoxin-beta receptor (LT-betaR), CD40, CD30, and LM
91 ult mice was reduced by systemic blockade of lymphotoxin-beta receptor (LTbeta R) signaling with a so
92 re NIK for activation of NF-kappaB, only the lymphotoxin-beta receptor (LTbeta-R) is expressed in mel
96 ammatory mechanism, including membrane-bound lymphotoxin-beta receptor (LTbetaR) and CXC chemokine re
98 r, which binds two known cellular receptors, lymphotoxin-beta receptor (LTbetaR) and the herpesvirus
99 this effect through the interaction with the lymphotoxin-beta receptor (LTbetaR) but not herpes virus
101 Moreover, we show that signals through the lymphotoxin-beta receptor (LTbetaR) in DC are also requi
102 R4-activated canonical NF-kappaB pathway and lymphotoxin-beta receptor (LTbetaR) induced non-canonica
107 equires innate lymphoid cells, which promote lymphotoxin-beta receptor (LTbetaR)-dependent maintenanc
110 SF-14) is a ligand of stromal cell-expressed lymphotoxin-beta receptor and T cell-expressed herpes vi
111 of six single chain-Fv fragments of the anti-lymphotoxin-beta receptor antibody, statistically signif
114 de development during embryogenesis involves lymphotoxin-beta receptor engagement and subsequent diff
115 al-associated lymphoid tissue by LTbetaR-Ig (lymphotoxin-beta receptor human Ig fusion protein) treat
116 nobese diabetic (NOD) mice were treated with lymphotoxin-beta receptor immunoglobulin fusion protein
117 CICD was strongly activated by both TNF and lymphotoxin-beta receptor ligation in IKKbeta-/- MEFs an
118 as well as pharmacological inhibition of the lymphotoxin-beta receptor markedly delays tumor developm
120 nd on activated lymphocytes and binds to the lymphotoxin-beta receptor, which is generally present on
121 on in the thymi of lymphotoxin-deficient and lymphotoxin-beta receptor-deficient mice contributes to
123 ions including BO, and that treatment with a lymphotoxin-beta receptor-immunoglobulin fusion protein
125 tion, BALB/c mice were treated in utero with lymphotoxin beta-receptor Ig fusion protein to generate
126 is factor superfamily member LIGHT activates lymphotoxin beta-receptor signaling, leading to the prod
127 activated, LTalphabeta(+), lymphocytes with lymphotoxin beta-receptor-expressing fibrosarcoma tumor
129 ated by intragraft TLOs and whether blocking lymphotoxin-beta-receptor (LTbetaR) signaling, a pathway
131 estingly, both the tumor necrosis factor and lymphotoxin beta receptors were down-regulated by NS5A.
134 tory cytokines, such as IL-1alpha, IL-1beta, lymphotoxin beta, TNFalpha, and IL-6, also increased.
135 colony-stimulating factor, stem cell factor, lymphotoxin beta, transforming growth factor beta1, and
136 eta (tumor necrosis factor/lymphotoxin-alpha/lymphotoxin-beta) triple knockout (KO) mice show a signi
138 kin (IL)-2, interferon-gamma (IFN-gamma) and lymphotoxin-beta, which mediate pro-inflammatory functio
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