Chemokines inhibitions

Methods for chemokine inhibition of cell-free virus infection on both primary and established cell lines are described in Subheadings 2.1. and 2.2. 

Chemokine Inhibition of HIV Infection of Primary PBMC and T-Cell Lines... 

Szabo I, Chen XH, Xin L, Adler MW, Howard OMZ, Oppenheim JJ, Rogers TJ (2002) Heterologous desensitization of opioid receptors by chemokines inhibits chemotaxis and enhances the perception of pain. Proc Natl Acad Sci USA 99 10276-10281. 

G. Acetylchohne, a-adrenergic amines, many neurotransmitters, chemokines Inhibits adenylate cyclase... 

E. CXCR3, Putative Receptor for IFN-Inducible (ELR ) CXC Chemokine Inhibition of Angiogenesis... 

SECRET domain VARV, ECTV, CPXV Secreted, protein domain fused to the TNFRs CrmB and CrmD, or expressed independently as three SCPs encoded by different genes, binds a limited set of CC and CXC chemokines, inhibits cell migration 42... 

Tak, P.P. (2005) Chemokine inhibition in inflammatory arthritis. Best Practice C Research. Clinical Rheumatology, 20, 929-939. 

Koenen, R.R. et al. (2009) Disrupting functional interactions between platelet chemokines inhibits atherosderosis in hyperlipidemic mice. Nature Medicine, 15, 97-103. 

Figure 16.1 Mechanisms of chemokine inhibition by the CKBPs encoded by pathogens. Chemokines interact with CACs present at the surface ofendothelial cells and are presented to the leukocytes. The chemokine receptors expressed at the surface of leukocytes interact with chemokines and intracellular signaling is triggered to induce cell migration. The CKBPs may have broad chemokine binding specificity, such as the poxvirus 35-kDa protein, the gammaherpesvirus M3 protein orthe MYXVM-...

As described before, chemokine inhibition may be a useful approach for the prevention of restenosis after coronary surgery or atherosclerosis. This concept has been further substantiated in vivo through the use of the broad spectrum vCKBP M3. Thus, systemic M3 expression from a transgene, or delivery of recombinant M3 protein, have been shown to reduce intimal hyperplasia after femoral artery injury [40] and aortic allograft transplantation [25], respectively. 

Bursill, C.A., McNeill, E., Wang, L., Hibbitt, O.C., Wade-Martins, R., Paterson, D.J., Greaves, D.R., and Channon, KM. (2009) Lentiviral gene transfer to reduce atherosclerosis progression by long-term CC-chemokine inhibition. 

Hayashi, S., Kurdowska, A., Cohen, A. B., Stevens, M. D., Fujisawa, N., and Miller, E. J. (1997) A synthetic peptide inhibitor for alpha-chemokines inhibits the growth of melanoma cell lines. J. Clin. Invest. 99,2581-2587. 

Bursill et al. (2004) used adenoviral-mediated gene transfer to express a soluble broad spectrum CC-chemokine inhibitor, 35K, and they examined its efficacy in mediating atherosclerotic lesion formation. In mice expressing the soluble 35K inhibitor, atherosclerotic lesion size was reduced by 55%, and this was accompanied by an 85% decrease in macrophage recruitment. This report confirmed the involvement of CC chemokines in the initiation and progression of lesion development and demonstrated that broad-spectrum CC-chemokine inhibition is a rational therapeutic target. 

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