ライフサイエンスコーパス: inflamed site

1 XP3(-) Treg-like cells uniquely populate the inflamed site.

2 pendent on rapid localization of MSCs to the inflamed site.

3 nsertion of mechanosensitive elements at the inflamed site.

4 evolution of the selected repertoire at the inflamed site.

5 finally within the peritoneum, the original inflamed site.

6 i-inflammatory and analgesic efficacy at the inflamed site.

7 pographic commitment of T cells for skin and inflamed sites.

8 both recruitment and increased longevity at inflamed sites.

9 primary responding B cells, and migrated to inflamed sites.

10 trol of spatial positioning of leukocytes at inflamed sites.

11 he spatial positioning of neutrophils within inflamed sites.

12 e LN and precise effector T cell delivery to inflamed sites.

13 and eosinophilic recruitment to resting and inflamed sites.

14 f M(phi) controls on resident cell number at inflamed sites.

15 ore control the mesangial cell complement at inflamed sites.

16 itial phase of immunoctye extravasation into inflamed sites.

17 ascular cell adhesion molecule-1 (VCAM-1) at inflamed sites.

18 nd an increase in macrophage accumulation at inflamed sites.

19 riminate between progressive and stable, but inflamed, sites.

20 egress of Ag-sequestered Th1 cells from the inflamed site and alleviated inflammation.

21 xis of M0 or M2 phenotype macrophages to the inflamed site and induce M2 phenotype polarization local

22 by controlling neutrophil recruitment to the inflamed site and survival and function therein.

23 thotrexate, enhances adenosine release at an inflamed site and that adenosine diminishes inflammation

24 gs relies on their capacity to accumulate at inflamed sites and appropriately adapt to their local en

25 trophils are the first immune cells to reach inflamed sites and contribute to the pathogenesis of chr

26 mmation by preventing macrophage egress from inflamed sites and is required for osteoclast differenti

27 a byproduct of impaired fluid drainage from inflamed sites and thus we provide a model unifying D6 f

28 required for their ability to accumulate at inflamed sites and to maintain high levels of Foxp3 expr

29 hat expression of the peptide is enhanced in inflamed sites, and that post-transcriptional regulatory

30 phocyte homing and neutrophil recruitment to inflamed sites are normal.

31 is not mediated by neural signaling from the inflamed site, as previously suggested, but is dependent

32 ion to accumulate and become inserted at the inflamed site, causing AMS.

33 current pneumonia occurred in the previously inflamed site, CD11/CD18 was not required.

34 uggest that in human CD4(+) T cells from the inflamed site, CD39 can be highly expressed on two popul

35 opose that subsequent Treg expansions at the inflamed site creates an environment that leads to compe

36 d their histotoxic contents are cleared from inflamed sites during resolution.

37 Effector T cell migration into inflamed sites greatly exacerbates tissue destruction an

38 nucleoside that is elaborated at injured and inflamed sites, has a central role in the regulation of

39 ession in biopsies from small bowel and from inflamed sites, implicating LIGHT as a mediator of mucos

40 5 and FOXP3 is frequently dissociated at the inflamed site in patients with juvenile idiopathic arthr

41 d for activated T cell extravasation into an inflamed site in vivo in mice.

42 t interleukin-23-interleukin-17 signature at inflamed sites in humans with LAD1 and in mouse models o

43 y evaluate kyn metabolism in local tissue or inflamed sites in humans, our data demonstrates that O(2

44 ected epithelial cells and their presence at inflamed sites in the genital tract will help understand

45 evidence that macrophage emigration from the inflamed site is controlled and demonstrates that this i

46 Neutrophil migration to inflamed sites is crucial for both the initiation of inf

47 e analog) and by local administration at the inflamed site of monoclonal antibody 3-E7, which recogni

48 NE is overexpressed at inflamed sites of viral infection.

49 significantly different between healthy and inflamed sites (P <0.05).

50 ontrast, analysis of cellular recruitment to inflamed sites provides evidence of specificity of recep

51 re, will generally be less effective at more inflamed sites, providing a rationale for the very high

52 These cells are more numerous at inflamed sites, so it is reasonable to expect clarithrom

53 s diverted Tfh cells from systemic (non-gut) inflamed sites such as the lung into the gut-associated

54 chemokine receptors that direct migration to inflamed sites, such as CCR2, CX3CR1, and CCR5, in TPH c

55 ty of tooth and implant-associated plaque at inflamed sites suggests that infected teeth are sources

56 Of relevance to the inflamed site, the ability of TNF-alpha to accelerate ap

57 44 together with VLA-4 fail to traffic to an inflamed site, thereby defining a discrete biological ro

58 gration of monocyte-derived cells out of the inflamed site through nearby lymphatic vessels.

59 ic signals to direct neutrophil migration to inflamed sites through its receptor BLT1.

60 ation can cause axons conducting through the inflamed site to become mechanically sensitive.

61 stem, impairing fluid and cellular flow from inflamed sites to lymph nodes and reducing efficiency of

62 Human gingival tissues from noninflamed and inflamed sites were also analyzed by RT-PCR.

63 ventional T cells, in blood, and also at the inflamed site, where they are clonally expanded.

64 ining immune cells migrate preferentially to inflamed sites, where they release beta-endorphin which

65 gan communication between the BM and distant inflamed sites, whereby a certain subset of multipotent

66 e defense when cell death occurs at infected inflamed sites while promoting later resolution with dim

67 es compared to SRP alone in the treatment of inflamed sites with >/= 5 mm PD.