ライフサイエンスコーパス: ILC1

1 ILC1 subsets may contribute to the inflammatory bowel di

2 ILC1, ILC2, and ILC3 cells were cultured for 5 days with

3 ILC1-derived interferon-gamma was necessary and sufficie

4 e inducer (LTi), and innate lymphoid cell 1 (ILC1) cells, but not ILC2 or ILC3 cells, were enriched i

5 s, liver innate lymphoid cells (ILC) type 1 (ILC1s) have been shown to represent a distinct lineage t

6 Adipose ILC1s were dependent on the transcription factors Nfil3

7 sis of parabiotic mice revealed that adipose ILC1s maintained long-term tissue residency.

8 While SMAD4 deficiency did not affect ILC1 differentiation, NK cells unexpectedly acquired an

9 Although all ILC1 subsets shared characteristics with Th1 cells, CD4(

10 entiation, NK cells unexpectedly acquired an ILC1-like gene signature and were unable to control tumo

11 stered within inflamed areas and acquired an ILC1-like phenotype.

12 nabled the conversion of these cells into an ILC1 phenotype in response to IL-12.

13 ersial whether natural killer (NK) cells and ILC1 cells are distinct cell types.

14 ILCs had characteristic of both NK cells and ILC1.

15 NK cells and ILC1s are developmentally distinct but share so many fea

16 oups of innate lymphoid cells (ILCs) such as ILC1, ILC2, and ILC3 populate the intestine, but how the

17 tor GATA-3 and a concomitant switch to being ILC1 cells that produced interferon-gamma (IFN-gamma).

18 s were also differentially expressed between ILC1s and cNKs, indicating that PLZF together with other

19 hared characteristics with Th1 cells, CD4(+) ILC1 also demonstrated significant phenotypic and functi

20 We also show that the frequencies of CD4(+) ILC1 and NKp44(+) group 3 ILC, but not CD4(-) ILC1 or gr

21 rmore, we demonstrate that CD4(+) and CD4(-) ILC1 are functionally divergent based on their IL-6Ralph

22 and functional features of CD4(+) and CD4(-) ILC1 suggest that they may have differing roles in the p

23 LC1 and NKp44(+) group 3 ILC, but not CD4(-) ILC1 or group 2 ILC, are increased in the peripheral blo

24 m+) ILCs acquire an natural killer (NK) cell/ILC1-like phenotype.

25 natural killer cells and helper-like cells (ILC1, ILC2 and ILC3).

26 issue-resident type 1 innate lymphoid cells (ILC1) serve an essential early role in host immunity thr

27 e recently identified innate lymphoid cells (ILC1, ILC2, and ILC3), and innate-like lymphocytes, incl

28 at distinguish type 1 innate lymphoid cells (ILC1s) from natural killer (NK) cells is a gene signatur

29 (NK) cells and type 1 innate lymphoid cells (ILC1s).

30 We were not able to detect ILC1 cells in any of the tissues assessed, however, we i

31 d cytokine-producing helper-like ILCs (i.e., ILC1s, ILC2s, ILC3s).

32 Three ILC classes have emerged, ILC1, ILC2 and ILC3, with ILC1 and ILC3 including severa

33 tance, loss of IFN-gamma or T-bet-expressing ILC1s in Rag1(-/-) mice increased susceptibility to C. d

34 s tumor growth, whereas intestinal Rorc(fm-) ILC1s or NK cells fail to inhibit tumor progression.

35 s for some ILCs and overlapping patterns for ILC1 cells and NK cells, whereas other ILC subsets remai

36 These data demonstrate a critical role for ILC1s in defense against C. difficile.

37 ad reduced numbers of antiviral IFN-gamma(+) ILC1 and increased numbers of immunopathologic IL-5(+) a

38 e of Immunity, identify T-bet(+)IFN-gamma(+) ILC1 that accumulate in the inflamed intestine of IBD pa

39 ls, interferon gamma-positive (IFN-gamma(+)) ILC1s, interleukin (IL)-13(+) ILC2s, and for IL-22(+), b

40 Here we characterized a human ILC1 subset that produced interferon-gamma (IFN-gamma) i

41 however, we identified intra-epithelial (ie)ILC1-like cells that represent a broader category of NK

42 we identify a subset of adipose group 1 ILC (ILC1) and demonstrate a role for these cells in metaboli

43 he subset previously defined as group 1 ILC (ILC1) contains CD4(+) CD8(-), CD4(-) CD8(+), and CD4(-)

44 f T-bet(+) IFN-gamma-producing group 1 ILCs (ILC1 and natural killer cells), CD8(+) cytotoxic T cells

45 ators of mucosal immunity, and group 1 ILCs (ILC1 cells) and group 3 ILCs (ILC3 cells) have been show

46 Group 1 ILCs (ILC1s) produce interferon gamma and depend on Tbet, grou

47 -5 and IL-13 in ILC2 cells, and IFN-gamma in ILC1 and ILC3 cells.

48 reciated cytokine-secreting cells, including ILC1 (IFN-gamma-expressing NK cells), ILC2 (IL-5 and IL-

49 by a Th1 response activated by infiltrating ILC1, NK, and LTi cells.

50 tably, IL-12 converted human ILC2 cells into ILC1 cells, and the frequency of ILC1 cells in patients

51 e ILCs can be phenotypically classified into ILC1, ILC2 and ILC3 subsets, the transcriptional control

52 l phenotype (ftILCPs) and differentiate into ILC1s, ILC2s and ILC3s in vitro.

53 Intraepithelial ILC1 were amplified in Crohn's disease patients and cont

54 well as liver and intestinal intraepithelial ILC1 have markers that denote tissue residency and trans

55 In mice, intraepithelial ILC1 were distinguished by CD160 expression and required

56 T cells share this profile, intraepithelial ILC1 may be their innate counterparts.

57 eptor-alpha, indicating that intraepithelial ILC1 are distinct from conventional NK cells.

58 Thus, intraepithelial ILC1 may initiate IFN-gamma responses against pathogens

59 Ablation of Zfp683-dependent liver ILC1 lead to increased viral load in the presence of int

60 rsor stage, by transient expression of mixed ILC1, ILC2 and ILC3 transcriptional patterns, whereas, i

61 were committed ILC progenitors with multiple ILC1, ILC2 and ILC3 potential at the clonal level.

62 was essential for the normal development of ILC1 and ILC3 cells but not of ILC2 cells.

63 r in the lineage-specific differentiation of ILC1 and ILC3 cells.

64 Raggammac(-/-) mice upregulate expression of ILC1- or ILC3-associated proteins following C. difficile

65 cells into ILC1 cells, and the frequency of ILC1 cells in patients with chronic obstructive pulmonar

66 studies have discovered the heterogeneity of ILC1 and ILC3 in the gastrointestinal tract.

67 We found that reconstitution of ILC1, ILC2, and NCR(-)ILC3 was slow compared with that o

68 Although a limited set of ILC1 genes depended on PLZF for expression, characterist

69 Runx3 controlled the survival of ILC1 cells but not of ILC3 cells.

70 elf, controlled the identity and function of ILC1s by promoting chromatin accessibility and depositio

71 e iNK stage, with a striking predominance of ILC1s over cNKs early in ontogeny.

72 we studied the developmental progression of ILC1s and demonstrated substantial overlap with stages p

73 Only ILC1 and ILC3, but not ILC2, undergo the RA-dependent ho

74 reversibly give rise to IFN-gamma-producing ILC1, plasticity of human or mouse ILC2 has not been sho

75 conventional dendritic cells (cDC1) promoted ILC1 production of IFN-gamma in a STAT4-dependent manner

76 Thus, adipose-resident ILC1s contribute to obesity-related pathology in respons

77 eration and accumulation of adipose-resident ILC1s in a manner dependent on the IL-12 receptor and ST

78 ct groups based on their cytokine secretion: ILC1 produce IFN-gamma, ILC2 secrete IL-5 and IL-13, and

79 ffector programs specific to the ILC subsets ILC1, ILC2 and ILC3 was initiated later, at the common I

80 er IFN-gamma-producing lineages such as Th1, ILC1, and intraepithelial gammadelta T cells.

81 ey originated from different precursors, the ILC1 and cNK lineages followed a parallel progression at

82 C precursor (ILCP) strictly committed to the ILC1, ILC2, and ILC3 lineages.

83 Mechanistically, these ILC1 cells augmented virus-induced inflammation in a man

84 Thus, ILC1 contribute an essential role in viral immunosurveil

85 urrent knowledge of NK cells and the various ILC1 subsets.

86 as the switch that determined an ILC2-versus-ILC1 response.

87 We studied mice in which ILC1s and NK cells lacked SMAD4, a signal transducer tha

88 SERPINB4 mRNA (both P < .0005) compared with ILC1.

89 sses have emerged, ILC1, ILC2 and ILC3, with ILC1 and ILC3 including several subsets.

90 Together with ILC1s, NK cells constitute group 1 ILCs, which are chara