ライフサイエンスコーパス: BALT

1 BALT HEVs also express the L-selectin ligand PNAd.

2 BALT most often accompanied A0 or A1 rejection.

3 BALT was found from 9 days to 2431 days after transplant

4 BALT-like lesion formation in the lungs of SE2(-/-) mice

5 literans developed in 29% of patients with a BALT-positive biopsy, a percentage not different from th

6 lished infection with oxytetracycline caused BALT, but not the lymphatics, to regress.

7 ts had transbronchial biopsies demonstrating BALT.

8 ce treated with P. aeruginosa (P.a.) develop BALT but B cell follicles lack FDCs while still harborin

9 nd adhesion molecules that are essential for BALT induction, organization, and maintenance.

10 endent induction and maturation pathways for BALT formation.

11 Toll-like receptor pathways are required for BALT induction by P.a., but not MVA, and provide evidenc

12 show that high endothelial venules (HEVs) in BALT express substantial levels of VCAM-1, in marked con

13 LPS-bead(+) cells were present in BALT, suggesting local induction of immune responses.

14 e migration pathways and immune responses in BALT and other bronchopulmonary tissues.

15 rmore, in IL-17-deficient mice, P.a.-induced BALT largely lacks B cells as well as CXCL12-expressing

16 ich seem to be initiated at sites of induced BALT (iBALT).

17 Inducible BALT (iBALT) can amplify pulmonary or systemic inflammat

18 Inducible BALT (iBALT) is associated with immune responses to resp

19 This IL-4/IL-13-dependent inducible BALT model will be useful for investigating the pathophy

20 ome; mucus plugging; and extensive inducible BALT.

21 n mice leads to the development of inducible BALT (iBALT), which is located in peribronchial, perivas

22 des that recruit lymphocytes from blood into BALT.

23 block the homing of B and T lymphocytes into BALT, whereas anti-alpha4 integrin and anti-VCAM-1 mAbs

24 ungs of naive mice and humans typically lack BALT, pulmonary infection in mice leads to the developme

25 The association of BALT with high-grade acute cellular rejection and with t

26 inal centers consistent with descriptions of BALT.

27 ed at random to evaluate the distribution of BALT lymphocyte subsets immunohistochemically.

28 Immunohistochemical examination of BALT showed helper T cells predominated over cytotoxic T

29 R-2/VEGFR-3 did not prevent the formation of BALT.

30 ansplant procedure and the identification of BALT.

31 required for the formation and maturation of BALT.

32 raises the possibility that the presence of BALT on transbronchial biopsy may be part of the evoluti

33 ymphatic network is restricted to regions of BALT, but lymphatics do not regress when BALT regresses

34 VA) is sufficient to induce highly organized BALT with densely packed B cell follicles containing a n

35 of the bronchus-associated lymphoid tissue (BALT) and infiltration of the pulmonary interstitium wit

36 such as bronchus-associated lymphoid tissue (BALT) in the lung, develops spontaneously at sites of ch

37 Bronchus-associated lymphoid tissue (BALT) is occasionally found in the lungs of mice and hum

38 Bronchus-associated lymphoid tissue (BALT) participates in airway immune responses.

39 grafts, bronchus-associated lymphoid tissue (BALT) plays a major role in the induction and persistenc

40 Bronchus-associated lymphoid tissue (BALT) was originally described as a mucosal lymphoid org

41 sion of bronchus-associated lymphoid tissue (BALT), goblet cell hyperplasia, epithelial hypertrophy,

42 ions of bronchus-associated lymphoid tissue (BALT), where VEGF-C-producing cells were scattered in T-

43 sembled bronchus-associated lymphoid tissue (BALT).

44 ry phenotype) but not naive T and B cells to BALT.

45 FA-1, targets specific lymphocyte subsets to BALT.

46 of BALT, but lymphatics do not regress when BALT regresses after antibiotic treatment.

47 he clinical and histologic associations with BALT identified on transbronchial biopsy in human lung a