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1 ands, including those that bind CD30 and the lymphotoxin beta receptor.
2 that CD30 signals predated those through the lymphotoxin beta receptor.
3 IGHT receptors herpesvirus entry mediator or lymphotoxin beta receptor.
4 75 neurotrophin receptor and weakly with the lymphotoxin-beta receptor.
5 to the cytosolic domains of CD30, CD40, and lymphotoxin-beta receptors.
7 f lymphotoxin was confirmed, as the use of a lymphotoxin beta receptor agonist results in partial res
9 us-host disease model, Treg cells expressing lymphotoxin beta receptor-AIR, which can be activated by
10 both of its identified signaling receptors, lymphotoxin beta receptor and herpes virus entry mediato
11 rmation was dependent on lymphotoxin and the lymphotoxin beta receptor and independent of lymphocytes
12 LIGHT protected mice from colitis via the lymphotoxin beta receptor and was expressed mainly by my
13 SF-14) is a ligand of stromal cell-expressed lymphotoxin-beta receptor and T cell-expressed herpes vi
14 of six single chain-Fv fragments of the anti-lymphotoxin-beta receptor antibody, statistically signif
15 y member 14 (TNFRSF14, also called HVEM) and lymphotoxin beta receptor are receptors for LIGHT that w
16 ts receptors, herpesvirus entry mediator and lymphotoxin beta receptor, are found in T cells and stro
19 ion of LT and LIGHT signaling with a soluble lymphotoxin beta receptor decoy protein attenuated the d
20 tinal inflammation when transferred into the lymphotoxin beta receptor-deficient mice, and herpes vir
21 on in the thymi of lymphotoxin-deficient and lymphotoxin-beta receptor-deficient mice contributes to
22 lymphoplastic (aly/aly) or splenectomized B6 lymphotoxin-beta receptor-deficient mice demonstrated th
23 de development during embryogenesis involves lymphotoxin-beta receptor engagement and subsequent diff
25 activated, LTalphabeta(+), lymphocytes with lymphotoxin beta-receptor-expressing fibrosarcoma tumor
26 , herpesvirus entry mediator (TNFRSF14), and lymphotoxin beta receptor, form an immune regulatory net
27 al-associated lymphoid tissue by LTbetaR-Ig (lymphotoxin-beta receptor human Ig fusion protein) treat
28 tion, BALB/c mice were treated in utero with lymphotoxin beta-receptor Ig fusion protein to generate
29 belonging to the TNF superfamily, by soluble lymphotoxin beta receptor-Ig (LTbetaR-Ig) inhibits the c
30 Blockade of LIGHT by its soluble receptors, lymphotoxin beta receptor-Ig or HVEM-Ig, inhibits the in
33 nobese diabetic (NOD) mice were treated with lymphotoxin-beta receptor immunoglobulin fusion protein
34 d state, blockade of this stimulation with a lymphotoxin beta receptor-immunoglobulin fusion protein
35 ions including BO, and that treatment with a lymphotoxin-beta receptor-immunoglobulin fusion protein
37 s receptors, herpes virus entry mediator and lymphotoxin beta receptor, it activates inflammatory res
38 CICD was strongly activated by both TNF and lymphotoxin-beta receptor ligation in IKKbeta-/- MEFs an
39 eatment with interferon-gamma, which induced lymphotoxin beta receptor (LT beta R) expression, was re
40 implex virus entry mediator (HVEM) and LIGHT/lymphotoxin beta receptor (LT beta R) interactions decre
42 is study demonstrates enhanced expression of lymphotoxin beta receptor (Lt betaR) during the demyelin
43 Recent studies revealed that the lymphotoxin/lymphotoxin beta receptor (LT)/LTbetaR system activates
46 4 interacts with the cytosolic domain of the lymphotoxin-beta receptor (LT beta R) and weakly with th
47 Here we report that blocking LT alpha beta/lymphotoxin-beta receptor (LT beta R) interaction in viv
49 hese clones encode the cytoplasmic domain of lymphotoxin-beta receptor (LT betaR), which is a member
50 osis factor-alpha (TNF-alpha), whereas decoy lymphotoxin-beta receptor (LT-betaR) fusion protein had
51 nsduction of the TNF receptor 2 (TNFR2), the lymphotoxin-beta receptor (LT-betaR), CD40, CD30, and LM
52 ult mice was reduced by systemic blockade of lymphotoxin-beta receptor (LTbeta R) signaling with a so
53 re NIK for activation of NF-kappaB, only the lymphotoxin-beta receptor (LTbeta-R) is expressed in mel
55 ediated by at least two receptors, including lymphotoxin beta receptor (LTbetaR) and herpes simplex v
56 cells including HT29 cells that express both lymphotoxin beta receptor (LTbetaR) and HVEM/TR2 recepto
57 tosis of various tumor cells expressing both lymphotoxin beta receptor (LTbetaR) and TR2/HVEM recepto
59 or receptors (TNFRs) as a homotrimer and via lymphotoxin beta receptor (LTbetaR) as a heterotrimeric
61 eady-state and after bone marrow transplant, lymphotoxin beta receptor (LTbetaR) controls entry of T
63 onditional gene-deficient mice, we find that lymphotoxin beta receptor (LTbetaR) directly controls th
66 (LT)alpha(1)beta(2) on inducer cells and the lymphotoxin beta receptor (LTbetaR) on stromal cells ini
67 dy sought to determine whether signaling via lymphotoxin beta receptor (LTbetaR) or herpesvirus entry
68 fusion protein between the IgG Fc domain and lymphotoxin beta receptor (LTbetaR) reduces lung fibrosi
71 tor (TNF) receptor superfamily members CD40, lymphotoxin beta receptor (LTbetaR), and B-cell-activati
72 bind the cytoplasmic domains of CD40 and the lymphotoxin beta receptor (LTbetaR), both of which are k
73 inflammation mediated by LIGHT, a ligand for lymphotoxin beta receptor (LTbetaR), not only stimulates
74 fic deletion of the thymus medulla regulator lymphotoxin beta receptor (LTbetaR), we show that thymic
75 a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration
87 ammatory mechanism, including membrane-bound lymphotoxin-beta receptor (LTbetaR) and CXC chemokine re
89 r, which binds two known cellular receptors, lymphotoxin-beta receptor (LTbetaR) and the herpesvirus
90 this effect through the interaction with the lymphotoxin-beta receptor (LTbetaR) but not herpes virus
92 Moreover, we show that signals through the lymphotoxin-beta receptor (LTbetaR) in DC are also requi
93 R4-activated canonical NF-kappaB pathway and lymphotoxin-beta receptor (LTbetaR) induced non-canonica
94 Here, we show that signaling through the lymphotoxin-beta receptor (LTbetaR) is critical for kidn
99 vation of innate immune effectors, STING and lymphotoxin-beta receptor (LTbetaR), results in CD8(+) T
100 equires innate lymphoid cells, which promote lymphotoxin-beta receptor (LTbetaR)-dependent maintenanc
103 ated by intragraft TLOs and whether blocking lymphotoxin-beta-receptor (LTbetaR) signaling, a pathway
104 nt region of IgG and extracellular domain of lymphotoxin beta receptor (LTbetaRIg) interrupted clonal
107 as well as pharmacological inhibition of the lymphotoxin-beta receptor markedly delays tumor developm
109 xin axis, and pharmacological stimulation of lymphotoxin beta receptor might represent a novel therap
110 s, herpesvirus entry mediator on T cells and lymphotoxin beta receptor on stromal cells, are implicat
112 lary epithelial cells of mice lacking either lymphotoxin beta receptor or the lymphotoxin alpha-chain
113 ory distress, and shows that blockade of the lymphotoxin beta receptor pathway reverses the disease.
116 mphangiogenesis in the thyroid and implicate lymphotoxin beta receptor signaling in this process.
117 Notch-dependent Esam(hi) DC subset required lymphotoxin beta receptor signaling, proliferated in sit
118 is factor superfamily member LIGHT activates lymphotoxin beta-receptor signaling, leading to the prod
122 found that an agonistic antibody against the lymphotoxin beta receptor was able to facilitate liver r
123 estingly, both the tumor necrosis factor and lymphotoxin beta receptors were down-regulated by NS5A.
124 e protein binds to the cytoplasmic domain of lymphotoxin beta receptor, which is a member of tumor ne
125 nd on activated lymphocytes and binds to the lymphotoxin-beta receptor, which is generally present on
126 oid cells through interactions with LTbetaR (lymphotoxin beta receptor), without the requirement for