CD11a Expression and soluble ICAM-1 levels in peripheral blood in high-risk and overt type 1 diabetes subjects

Myśliwiec, Janusz; Krętowski, Adam; Kinalski, Maciej; Kinalska, I

doi:10.1016/s0165-2478(99)00133-9

Cited by 28 publications

(26 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increasing evidence supports the role of plasma levels of the CAMs (sICAM-1, sVCAM-1, and E-selectin) as emerging biomarkers of atherosclerosis (40) (44) suggest that sICAM-1 levels are significantly elevated in type 1 diabetic patients and, in fact, are increased to a greater extent in preclinical diabetes compared with in overt diabetes. In our study, we also showed that sICAM levels are significantly increased in type 1 diabetes without macrovascular complications.…”

Section: Discussionmentioning

confidence: 98%

Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Glaser²,

et al. 2006

View full text Add to dashboard Cite

, and monocyte function). High-sensitive CRP, soluble intracellular adhesion molecule (sICAM), sCD40L, and nitrotyrosine levels were significantly elevated in type 1 diabetic subjects compared with in control subjects (P < 0.05). Monocyte superoxide anion release was significantly increased in the resting (37%; P < 0.05) and activated state (26%; P < 0.005) in type 1 diabetic compared with in control subjects. Monocyte interleukin (IL)-6 levels were significantly elevated in type 1 diabetic subjects compared with in control subjects in the resting state (51%; P < 0.05) and after lipopolysaccharide activation (31%; P < 0.01). Monocyte IL-1␤ levels were increased in the activated monocytes in type 1 diabetic compared with in control subjects. There were no significant differences in monocyte tumor necrosis factor levels or adhesion between the two groups. Thus type 1 diabetes is a proinflammatory state, as evidenced by increased levels of monocyte IL-6, superoxide anion, and plasma CRP, sICAM, sCD40L, and nitrotyrosine levels. These results have a major implication on our understanding of the role of inflammation in vasculopathies in type 1 diabetes. Diabetes 55: 774 -779, 2006

show abstract

Section: Discussionmentioning

confidence: 98%

Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Glaser²,

et al. 2006

View full text Add to dashboard Cite

show abstract

“…For example, anti-ICAM-1 and anti-CD11a monoclonal antibodies (mAb) have been shown to inhibit T-cell adhesion mediated by LFA-1 and have been developed for the treatment of rheumatoid arthritis, insulin-dependent diabetes, and psoriasis. 5,6 Also, small organic molecules such as lovastatin, 7 p-arylthiocinnamides, and hydantoin derivatives (i.e., BRIT-377) 8,9 have been shown to inhibit ICAM-1/LFA-1 interactions by binding to the I-domain of LFA-1.…”

mentioning

confidence: 99%

Inhibition of ICAM-1/LFA-1-mediated heterotypic T-cell adhesion to epithelial cells: design of ICAM-1 cyclic peptides

Anderson

Yakovleva

et al. 2004

Bioorganic & Medicinal Chemistry Letters

View full text Add to dashboard Cite

Abstract:In this work, we have designed cyclic peptides (cIBL, cIBR, cIBC, CH4 and CH7) derived from the parent IB peptide (ICAM-1 1-21 ) that are inhibitors of ICAM-1/LFA-1-mediated T-cell adhesion to Caco-2 cell monolayers. Cyclic peptide cIBR has the best activity of any of the peptides evaluated. The active ICAM-1 peptides have a common Pro-Arg-Gly sequence that may be important for binding to LFA-1. Graphic Abstract:Inhibition of LFA-1/ICAM-1-mediated Tcell adhesion by ICAM-1-derived peptides

show abstract

“…Interactions between adhesion molecules such as LFA-1 (CD11a/CD18) and ICAM-1 have an important role in insulitis in NOD mice and humans (Mysliwiec et al, 1999). ICAM-1/LFA-1 interactions are involved in leukocyte adhesion to vascular endothelium prior to infiltration of the islet.…”

Section: Blocking Icam-1/lfa-1 Interactionsmentioning

confidence: 99%

“…ICAM-1/LFA-1 interactions are involved in leukocyte adhesion to vascular endothelium prior to infiltration of the islet. Individuals with overt diabetes have high levels of CD11a on their monocytes and lymphocytes (Mysliwiec et al, 1999). Administration of anti-LFA-1 and anti-ICAM-1 mAbs to female NOD mice at 2 weeks of age completely prevented the development of spontaneous diabetes and formation of insulitis until 30 weeks of age (Moriyama et al, 1996).…”

Section: Blocking Icam-1/lfa-1 Interactionsmentioning

confidence: 99%

Peptides and Proteins for Treatment and Suppression of Type 1 Diabetes

Badawi¹,

Büyüktimkin²,

Kiptoo³

et al. 2011

Type 1 Diabetes - Pathogenesis, Genetics and Immunotherapy

View full text Add to dashboard Cite

CD11a Expression and soluble ICAM-1 levels in peripheral blood in high-risk and overt type 1 diabetes subjects

Cited by 28 publications

References 27 publications

Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Inhibition of ICAM-1/LFA-1-mediated heterotypic T-cell adhesion to epithelial cells: design of ICAM-1 cyclic peptides

Peptides and Proteins for Treatment and Suppression of Type 1 Diabetes

Contact Info

Product

Resources

About