1999
DOI: 10.1002/jlb.65.3.349
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Expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in acute and chronic inflammation

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Cited by 145 publications
(110 citation statements)
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“…Studies have shown that vascular adhesion molecules are important for T cell migration into islets, and TNF-TNFR1 signaling is important for upregulating the expression of adhesion molecules (33,34). However, we did not find decreased expression of vascular adhesion molecules in TNFR1-deficient mice.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Studies have shown that vascular adhesion molecules are important for T cell migration into islets, and TNF-TNFR1 signaling is important for upregulating the expression of adhesion molecules (33,34). However, we did not find decreased expression of vascular adhesion molecules in TNFR1-deficient mice.…”
Section: Discussionmentioning
confidence: 99%
“…4A, 4B). TNF-TNFR1 signaling upregulates the expression of important adhesion molecules such as MAdCAM-1 and VCAM-1 (33). Previous studies have shown that blocking MAdCAM-1 and VCAM-1 in NOD mice prevents diabetes, demonstrating the importance of these adhesion molecules in T1D progression (34).…”
Section: Tnfr1 Deficiency Does Not Affect Priming Of Ag-specific T Cementioning
confidence: 97%
“…MAdCAM mRNA message has been detected in brain tissue 13 and pro-inflammatory cytokines can increase the expression of MAdCAM on brain-derived endothelial cells, 12 but most studies have not observed MAdCAM protein expression in the CNS. 10,11 In preclinical models, including experimental autoimmune encephalomyelitis, CNS MAdCAM expression has been observed 14 or reported to be absent 22,27,28 and the effects of blocking MAdCAM/␣ 4 ␤ 7 interactions on encephalomyelitis lesions have either been reported to be beneficial, [15][16][17] or without effect 22,23 and dependent on ␣ 4 ␤ 1 / VCAM interactions. In order, to address these contentions described in the preclinical literature and understand the potential role for MAdCAM in control and inflamed CNS tissue, we have characterized the protein expression of MAdCAM in human unaffected and MS brain tissue and compared this with that of VCAM.…”
Section: Discussionmentioning
confidence: 99%
“…35,36 Studies have implicated endothelial cell ICAM-1 and MadCAM-1 along with leukocyte a 4 b 1 (VLA-4) and a 4 b 7 expression as primary mediators of leukocyte recruitment in colitis. [37][38][39][40] However, other reports have clearly documented increased expression of b 2 integrins, including LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18), in Crohn's disease and ulcerative colitis suggesting that these molecules may also play an important role in governing chronic inflammation of the bowel. [41][42][43][44] Few studies have directly examined the role of these molecules during experimental colitis with these reports documenting modification of trinitrobenzene sulfonic acid (TNBS) colitis with anti-CD18 or CD11b/ CD18 antibodies.…”
Section: Discussionmentioning
confidence: 99%