Intracellular adhesion molecule

PAMPs and various tissue factors can prime DCs to produce T-cell-polarizing factors [21], IL-12 is a pro-inflammatory cytokine that induces IFN-y and promotes the development of Thl-cell differentiation [31], Other Thl-polarizing factors are IFN-a and IFN-(3 [32] and cell-surface expressed intracellular adhesion molecule (ICAM)-l [33]. On the other hand, it has been shown that NF-kB inducing kinase (NIK), which is known to regulate B-cell maturation and lymphoid organogenesis, is important for the induction of Thl7 cells [34],... 

Oxidatively modified LDL up-regulates the surfece expression of VCAM-1 and intracellular adhesion molecule-1 (ICAM-1) in cultured endothelial cells, promoting the interactions between both cell types (Kume et al., 1992). This may play a pivotal role in the development of atherosclerosis by promoting the penetration of circulating monocytes into the suben-dothelial space whilst inhibiting the mobility of resident macrophages. It has been previously demonstrated that ICAM-1, E-selectin, and VCAM-1 are up-regulated in the microvasculature of rheumatoid but not control synovium (Corkill et al., 1991 Koch et al., 1991). The association between ox-LDL and increased expression of adhesion molecules in the inflamed synovium has yet to be studied. 

An anti-intracellular adhesion molecule-1 (anti-ICAM-1) antibody reduced neurological damage in a rabbit embolic model of stroke followed by thrombolysis with tissue-type plasminogen activator (tPA). When thrombolysis was delayed for 3 h following embolism, neither tPA nor the tPA/ICAM combination reduced neurological damage. 

Levocabastine H,-receptor antagonist Downregulates intracellular adhesion molecules, decreasing the inflammatory response may be used for up to 2 weeks... 

ICAM-1 Intracellular adhesion molecule 1 (ICAM-1), an immunoglobulin, plays an important role in the transport and activation of leukocytes. In Crohn s disease (inflammation of the alimentary tract), there is an overexpression of ICAM-1, which causes inflammation. Laboratory studies show that antisense oligonucleotides can reduce the expression of ICAM-1 and hence inflammation. 

Cancer antigen overexpressed in adenocarcinoma Intracellular adhesion molecule Primarily pancreatic... 

Human rhinoviruses (HRV) are members of the Picornaviridae family. The HRVs are classified according to their receptor specificity into members of the major and minor groups. The 87 members of the major-group viruses bind to the intracellular adhesion molecule receptor 1 (ICAM-1), whereas the 12 serotypes of the minor group bind to members of the low-density lipoprotein receptor family (LDLR) [42]. Rhinoviruses cause more than a billion cases of the common cold each year and are also associated with asthma exacerbations [43,44]. Statistically, one encounters one to three infections per year on the average [45]. As a result, rhinoviral infections are responsible for 25 million days of missed work in the USA [46]. 

SECs, like the vascular endothehum, play an active part in the control of leucocyte recruitment in cases of acute and chronic inflammatory conditions. Eeucocyte recruitment from the blood compartment is a crucial determinant for the induction of immunity and inflammation. SECs control this process by producing cytokines that activate leucocytes and by expressing adhesion molecules. Under inflammatory conditions upregulation of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was found [35 36], as well as expression of E-selectin and P-selectin [37]. Together with the expression of CD4 on SECs it has been postulated that these adhesion molecules might also be involved in the adhesion of KC cells to the sinusoidal wall [20]. 

Cheng et al. showed that intravenous infusion of intracellular adhesion molecule (ICAM) AS-ODN markedly reduced ICAM-1 expression, alleviated infiltration of inflammatory cells and accumulation of extracellular matrix in the obstructed kidney of mice with unilateral obstruction of the ureter [133],... 

The intracellular adhesion molecule-1 (ICAM-1) is an important protein of endothelial cells. Its expression is induced by the proinflammatory cytokines IL-I, TNF-a, and INF-y during the early phase of the inflammatory process. Under these conditions, its soluble form, sICAM-1, is released intrathecally at a high rate, probably originating from the endothelial cells of the inflamed tissue (i.e., the meninges and adjacent brain parenchymal tissue). 

Psoriasis is a disease of the immune system that involves T lymphocytes. The etiology and pathogenesis of psoriasis results from complex communications that cause activation of T lymphocytes and trafficking to the skin. Further reactivation causes inflammation and overproduction of skin, resulting in lesions and plaques. In psoriatic skin, there is an upregulation of intracellular adhesion molecule-1 (ICAM-1) on endothelium and keratinocytes. 

SPLA2, secretory phospholipase A2 COX-2, inducible nitric oxide synthase iNOS, inducible nitric oxide synthase SOD, superoxide dismutase ICAM-1, intracellular adhesion molecule-1 VCAM-1, vascular adhesion molecule-1 TNF-a, tumor necrosis factor-a IL, interleukin and MMP, matrix metalloproteinases. 

Hydrophilic surfactant proteins A (SP-A) and D (SP-D), secreted by type II pneumocytes, interact specifically with a wide range of microorganisms and play important roles in the innate, natural defense system of the lung [16]. Both mRNA and protein levels of SP-A and SP-D increase dramatically in response to lung infection, injury and endotoxin challenge [17]. Type II pneumocytes also express class II major histocompatibility complex (MHC) antigens and intracellular adhesion molecule (ICAM-1), which may facilitate pulmonary immune responses [15]. 

Increases in plasma S-AA levels have previously been reported in patients with coronary disease (57). S-AA and plasma intracellular adhesion molecule-1 were elevated in patients with CAD and hyperhomocysteinemia, but only S-AA decreased after vitamin supplementation (35). Homocysteine activates nuclear factor- in endothelial cells, possibly via oxidative stress (58), and increases monocyte chemoattractant protein-1 expression in vascular smooth muscle cells (59). Additionally, it stimulates interleukin-8 expression in human endothelial cultures (60). These inflammatory factors are known to participate in the development of atherosclerosis. Taken together, these reports suggest an association of elevated tHcy and low-grade inflammation in CAD. 

Many mediators of inflammation have been identified— cytokines IL-6, tumor necrosis factor alpha cell adhesion molecules intracellular adhesion molecule-1 (ICAM-I), P-selectin and acute phase reactants CR.R fibrinogen, serum amyloid A, and soluble CD40 (Fig. I) (3). Myeloperoxidase is an enzyme secreted from monocytes, neutrophils, and macrophages. A single measurement taken from patient with chest pain in the emergency department predicted the early risk of myocardial infarction and the risk of major cardiac of ends in the next 30 days to six months (15). 

Kavanaugh, A. F., Schulze-Koops, H., Davis, L. S., and Lipsky, R E. (1997). Repeat treatment of rheumatoid arthritis patients with a murine anti-intracellular adhesion molecule 1 monoclonal antibody. Arthritis Rheum. 40, 849-853. 

Alicaforsen - Isis Pharmaceuticals Antisense oligonucleotide Phase 3 Inhibitor of intracellular adhesion molecule-1 (ICAM-1) Crohn s disease... 

Liu G, Huth JR, Olejniczak ET, Herdoza R, DeVries P, Lietza S, Reilly EB, Okosinski GF, Fesik SW, vonGeldern TW, Novel p-arylthio cinnamides as antagonists of leukocyte function-associated antigen-l/intracellular adhesion molecule-1 interaction. 2. Mechanism of inhibition and structure-based improvement of pharmaceutical properties, J. Med. Chem., 44 1202-1210, 2001. 

Williams et al. (1997) described renal ischemia-reperfusion injury in rats. The animals were anesthetized and subjected to 45min of bilateral renal occlusion using atraumatic vascular clamps before renal perfusion was reestablished. After various time interval (up to lweek) blood urea nitrogen, creatinine and myeloperoxidase activity in the kidney were determined. The protective effects of an intracellular adhesion molecule monoclonal antibody were tested. 

Hayashi et al. (1996) tested the effects of a flavonoid in original-type anti-glomerular basement membrane antibody associated glomerulonephritis in male Sprague Dawley rats on upregulation of intracellular adhesion molecule expression and on increase in leukocyte function-associated antigen positive cells in nephritic glomeruli. 

Figure 32.7. Mechanism underlying UVR-induced immune suppression. Uroconic acid, membrane lipids, and DNA are molecular targets. Langerhans cells and keratinocytes are the cellular targets. Mediators produced by skin cells have both local and systemic effects. Abbreviations MHC, major histocompatibility complex ICAM, intracellular adhesion molecule UCA, urocanic acid IL, interleukin PGE, prostaglandin E.

---