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1                      IFN-gamma and IL-17 are colitogenic.
2  and cohousing experiments revealed that the colitogenic activity of this microbiota is transferable
3  signaling in T cells that contribute to its colitogenic activity.
4 istone demethylase activity to dampen T cell colitogenic activity.
5 t influences bacterial populations to become colitogenic, and this colitis is communicable to genetic
6 terized by increased levels of mucolytic and colitogenic bacteria.
7 he host immune response as a way to identify colitogenic bacteria.
8      16S rRNA sequencing showed expansion of colitogenic Bacteroides sp. in Itch(-/-) mice.
9 ng epithelial reprograming and enhanced anti-colitogenic capacity.
10 litis by regulating neutrophil infiltration, colitogenic CD4(+) T cell activation, and proinflammator
11 - or dextran sulfate sodium-induced colitis, colitogenic CD4(+) T cells (T-helper 1 and Th17 cells) a
12 ith colitis, the local release of opioids by colitogenic CD4(+) T cells led to significant reduction
13                      We investigated whether colitogenic CD4(+) T cells that accumulate in the inflam
14 IRF4 expression in cDC2 in the generation of colitogenic CD4(+) T cells, which becomes redundant as c
15  lamina propria, and IFN-gamma production by colitogenic CD4(+) T cells.
16                                          The colitogenic Cdcs1 allele impairs innate immunity to bact
17 olonic fibrosis both spontaneously and under colitogenic conditions.
18 ression of toll-like receptors, and produced colitogenic cytokines, such as IL-6 and IL-23, after act
19 inal disease tolerance with implications for colitogenic diseases.
20 y stage of INT cells resulted in an impaired colitogenic effect of INT cells.
21 5(+) population is masked by the presence of colitogenic effector cells that cannot be suppressed.
22 t provokes pathological RelA activity in the colitogenic gut remains unclear.
23 olyposis pouch, the UC pouch was enriched in colitogenic immune cells even without inflammation.
24 he Enterobacteriaceae recently identified as colitogenic in a T-bet(-/-)Rag2(-/-) ulcerative colitis
25 utoimmune colitis and those activated during colitogenic infection are distinguishable populations ch
26 inflammatory roles of Treg in the context of colitogenic innate immune response during pathogenic bac
27 ow that high IgA coating uniquely identifies colitogenic intestinal bacteria in a mouse model of micr
28 e IL-23 receptor defines an IL-10-regulated, colitogenic memory CD4+ T cell subset that is poised to
29 phox-/- and gp91phox-/- mice that harbored a colitogenic microbiota had increased colitis severity, t
30 the impact of microbiota standardization and colitogenic microbiota transfer on mucosal immune respon
31  inflammation by supplying the gut with both colitogenic pathobionts and pathogenic T cells.
32 al and environmental factors, leading to pro-colitogenic perturbations of the host-commensal relation
33 r of the intestinal microbiome transfers the colitogenic phenotype from tryptophan starved animals to
34                             Supporting their colitogenic phenotype, CD161(+) Th17 cells were found in
35 the liver and the gut and shows a restricted colitogenic phenotype.
36 was required for the development of a highly colitogenic phenotype.
37 into the T(H)17 subset of helper T cells and colitogenic potential, in a manner dependent on transfor
38 iginal hypothesis, limits their survival and colitogenic potential.
39 ity to colitis, with increased prevalence of colitogenic Prevotellaceae strains and decreased immunor
40    This mechanism was investigated using the colitogenic, protease-secreting enteric microbe Enteroco
41                          A major C3H-derived colitogenic QTL (Cdcs1) on chromosome (Chr.) 3 contribut
42 The resistant B6 background also contributed colitogenic QTL: Cdcs4 (Chr. 8), Cdcs5 (Chr. 17, MHC), a
43 ies qualitative features of the IL-23-driven colitogenic response by negatively regulating IL-23R exp
44 ies T-bet as a key modulator of IL-23-driven colitogenic responses in the intestine and has important
45 on of Treg cells in the colon and control of colitogenic responses.
46 ated colitis in wild-type mice, confirming a colitogenic role for the endogenous RAS.
47  Lachnospiraceae) and a greater abundance of colitogenic strains (of the family Erysipelotrichaceae).
48 ed by intestinal resident Klebsiella oxytoca Colitogenic strains produce the nonribosomal peptides ti
49                             In conclusion, a colitogenic susceptibility QTL on Chr. 3 has been shown
50 GFP) (EGFP, enhanced GFP) was crossed to the colitogenic susceptible strain IL-10-/- and derived into
51 cell populations or whether the IL-23-driven colitogenic T cell program regulates upstream hematopoie
52 s of T cell-mediated colitis, TRPV1 promoted colitogenic T cell responses and intestinal inflammation
53 g T cell proliferation in vitro and Th1-type colitogenic T cell responses in vivo.
54 atory functions for IFN-gamma to orchestrate colitogenic T cell responses through its distinct action
55 ygyrus before reconstitution with IL-10(-/-) colitogenic T cells are protected from colitis.
56  commensal bacteria in the donor mice drives colitogenic T cells into the Ag-experienced/memory T cel
57 n whether they act to prevent the priming of colitogenic T cells or actively control these cells as p
58 , Bhlhe40+ GM-CSF+ CD4+ T cells constitute a colitogenic T-cell population that promotes indirect all
59                                     In mice, colitogenic Th1 and Th17 cells promote intestinal inflam
60 ed chronic enterocolitis via an imbalance of colitogenic Th1 cells and Treg cells.
61     Taken together, these data indicate that colitogenic Th1 cells enter into the Ag-experienced pool
62   In this study, we describe the presence of colitogenic Th1 cells within the CD4(+)CD45RB(low) popul
63                    As OX40 also promoted the colitogenic Th1 response, its expression on T reg cells
64           Anti-IL-23p19 induced apoptosis in colitogenic Th17 cells in vitro and in vivo.
65 eliminates inflammatory encephalitogenic and colitogenic Th17 cells, without substantially affecting
66 itis; however, a cellular mechanism by which colitogenic Th17 immunity arises in vivo remains unclear
67  T cells impaired mucosal iTreg and enhanced colitogenic Th17 responses in mice with CD4+ T cell-indu
68  mesenteric lymph nodes (mLNs), and limiting colitogenic Th17 responses.
69 ptive transfer model, Th9(KO) cells are less colitogenic than Th9(WT), whereas IL9 blockade diminishe