ライフサイエンスコーパス: ILF

1 ILF development was profoundly arrested in the absence o

2 ILF formation occurs in the absence of T lymphocytes and

3 Although ILF bound constitutively to the IL-2 promoter, it was no

4 -lateral preoccipital region projects via an ILF-SLF pathway to frontal area 8Av.

5 mscribed regions of the FF, PWMB, UF, AF and ILF.

6 nhemopoietic stromal cell networks in CP and ILF of adult mice also expressed FDC-M1, CD157 (BP-3), a

7 dentified VCAM-1(+) cells within both CP and ILF that are candidates for the stromal cells involved i

8 ce resulted in reconstitution of both CP and ILF.

9 r transfer to CD132-null mice lacking CP and ILF.

10 lesion in the location of the right IFOF and ILF.

11 and Ag-specific B lymphocyte responses, and ILF B lymphocytes express elevated levels of LT in the a

12 ient to restore the organization of CLPs and ILFs and host defense against infection with C. rodentiu

13 anization and maintenance of mature CLPs and ILFs in the colon during infection with Citrobacter rode

14 s) are components of cryptopatches (CPs) and ILFs and were therefore evaluated in this process.

15 Cs, whereas LTi-like ILCs, cryptopatches and ILFs were partially dependent on Notch signaling.

16 We also observed associations between ILF and fornix microstructure and category-selective BOL

17 sequences in the IL-2 promoter are bound by ILF and that this binding may be involved in the control

18 ontains clusters of DCs restricted to the CP/ILF continuum.

19 isual anatomy; (ii) the tractography-defined ILF is structurally distinct from fibres of the optic ra

20 ssential for their entry into the developing ILFs.

21 While the function of the direct ILF pathway is unclear, it appears to mediate the fast t

22 We observed that diverse ILF cellular populations express alpha(4)beta(7) and alp

23 ription factor IL-2 enhancer binding factor (ILF) is constitutively expressed in both resting and act

24 rt that interleukin enhancer binding factor (ILF)3, a double-stranded RNA binding protein, associates

25 eyed via the inferior longitudinal fascicle (ILF) to the parietal lobe (areas POa and IPd), superior

26 (MCP), the inferior longitudinal fasciculi (ILF), inferior frontooccipital fasciculi (IFOF), genu (G

27 d the right inferior longitudinal fasciculi (ILF).

28 the right inferior longitudinal fasciculus (ILF) (P = .0008).

29 the right inferior longitudinal fasciculus (ILF) and left forceps major (>/=164mul, p<.01) than age-

30 er tracts [inferior longitudinal fasciculus (ILF) and/or inferior fronto-occipital fasciculus (IFOF)]

31 s (AF) and inferior longitudinal fasciculus (ILF) as fiber tracts that connect regions already implic

32 ulus (AF), inferior longitudinal fasciculus (ILF), uncinate fasciculus (UF) and cingulum bundle (CB).

33 ent of the inferior longitudinal fasciculus (ILF).

34 the right inferior longitudinal fasciculus (ILF).

35 belled the inferior longitudinal fasciculus (ILF).

36 ructure of inferior longitudinal fasciculus (ILF, connecting occipital and ventro-anterior temporal l

37 the right superior longitudinal fasciculus, ILF, and forceps minor (>/= 164mul, p<.01).

38 l intestine, the isolated lymphoid follicle (ILF).

39 opment of CP or isolated lymphoid follicles (ILF) after transfer to CD132-null mice lacking CP and IL

40 atches (CP) and isolated lymphoid follicles (ILF) in the small intestine of C57BL/6 mice.

41 Isolated lymphoid follicles (ILFs) are organized lymphoid structures that facilitate

42 Isolated lymphoid follicles (ILFs) are recently appreciated members of the mucosal im

43 ches (CLPs) and isolated lymphoid follicles (ILFs) are two main lymphoid structures in the colon.

44 yptopatches and isolated lymphoid follicles (ILFs), but not embryonically 'imprinted' Peyer's patches

45 transform into isolated lymphoid follicles (ILFs), which subsequently act as sites for the generatio

46 mphoid tissues, isolated lymphoid follicles (ILFs).

47 ch of the two sequence elements required for ILF binding decreased IL-2 promoter activity when assaye

48 beta receptor-dependent events required for ILF formation can occur in adulthood and require LT-suff

49 examine the nature and factors required for ILF formation.

50 re the influx of B220+ B lymphocytes to form ILFs.

51 monstrate that that similar to PP formation, ILF formation requires lymphotoxin (LT)- and LT beta rec

52 Furthermore, ILF DCs express CXCL13, and depletion of DCs resulted in

53 ions of interest were placed on the SLF, IFO-ILF, and PLIC, and tensor metrics were calculated.

54 (P = .504), while mean FA values for the IFO-ILF (P = .009) and PLIC (P < .0001) were higher than tho

55 ncrease in mean axial diffusivity in the IFO-ILF in the control group but not in the dyslexia group.

56 t B lymphocytes in the formation of immature ILFs (loosely organized clusters of B lymphocytes), LT-s

57 are required for the progression of immature ILFs to mature ILFs (organized lymphoid aggregates with

58 B220(+) cells (which we have termed immature ILFs) to well-organized lymphoid nodules (which we have

59 sential role for alpha(4)beta(7)/MAdCAM-1 in ILF development corresponding to the influx of beta(7)-e

60 ing to intestinal lymphoid structures and in ILF development.

61 Concordant with a block in ILF development at a stage corresponding to the influx o

62 These results reveal DC participation in ILF transformation and maintenance and suggest that in p

63 In addition, expression of TRANCE in ILF was concentrated just beneath the follicle-associate

64 the chemokine CXCL13, CP transformation into ILF was arrested.

65 had lower fractional anisotropy in the left ILF (P = .02) than patients without visual hallucination

66 easures of word reading, while only the left ILF correlated with reading comprehension scores.

67 for lower white matter integrity in the left ILF, particularly for patients with a history of visual

68 ng the mean diffusion indices along the left ILF, patients had significantly reduced fractional aniso

69 driven positive-feedback loop driving mature ILF formation, mature ILFs express elevated levels of B

70 We demonstrate that mature ILF formation occurs in response to lumenal stimuli, inc

71 ck loop driving mature ILF formation, mature ILFs express elevated levels of B lymphocyte chemoattrac

72 ymphoid nodules (which we have termed mature ILFs).

73 r the progression of immature ILFs to mature ILFs (organized lymphoid aggregates with a follicle-asso

74 s, and the second site functions to modulate ILF binding.

75 Using murine ILF formation as a model, we have examined the roles of

76 CP but not ILF were present in the small intestine from NF-kappaB-i

77 inguished from the LT-dependent formation of ILF and Peyer's patches by not requiring the presence of

78 ated with strengthening (renormalization) of ILF MK (r = -0.90, p < 0.05 corrected), suggesting that

79 uctures fitting the previous descriptions of ILFs, ranging from clusters of B220(+) cells (which we h

80 ls) are indispensable for the development of ILFs.

81 otential role for CCR6 in the development of ILFs.

82 d depletion of DCs resulted in regression of ILFs and disorganization of CPs.

83 o lymphoid tissues containing lymphocytes or ILFs.

84 kills: the FA values for both left and right ILF were correlated with measures of word reading, while

85 nd precentral (T = 6.47) gyri, and one right ILF end point, the occipital lobe (T = 5.36).

86 nstead implicating only one tract, the right ILF, in the ASD phenotype.

87 row reconstitution studies demonstrated that ILF development is dependent on CCR6-sufficient B lympho

88 These observations indicate that ILFs contain Ag-naive lymphocytes, and suggest that even

89 These findings suggest that ILFs are organized intestinal lymphoid structures whose

90 The ILF DC population was distinguished from that of the lam

91 onsistent with classical descriptions of the ILF in man and with monkey visual anatomy; (ii) the trac

92 e in FA was found in MS patients in both the ILFs and IFOFs (p<0.001) and in the left MCP and right S

93 ng the LTi-like cells and lymphocytes, while ILF stromal cells and vessels within ILFs express VCAM-1

94 its ligand CCL20 are highly expressed within ILFs and that B lymphocytes are the largest CCR6-express

95 es, and suggest that events occurring within ILFs shape subsequent immune responses mediated by these

96 he largest CCR6-expressing population within ILFs.

97 , while ILF stromal cells and vessels within ILFs express VCAM-1 and MAdCAM-1, respectively.