CCL9
Chemokine (C-C motif) ligand 9(CCL9) is a smallcytokinebelonging to the CCchemokinefamily. It is also calledmacrophage inflammatory protein-1 gamma(MIP-1γ),macrophage inflammatory protein-related protein-2(MRP-2) and CCF18, that has been described in rodents. CCL9 has also been previously designatedCCL10,although this name is no longer in use. It is secreted byfollicle-associatedepithelium(FAE) such as that found aroundPeyer's patches,and attractsdendritic cellsthat possess the cell surface moleculeCD11band thechemokine receptorCCR1.[2]CCL9 can activateosteoclaststhrough its receptor CCR1 (the most abundant chemokine receptor found on osteoclasts) suggesting an important role for CCL9 inbone resorption.[3]CCL9 is constitutively expressed inmacrophagesandmyeloidcells.[4][5]Thegenefor CCL9 is located onchromosome11 in mice.[5]
CCL9 is a chemokine involved in the process of signaling an antileukemic response and is a potential form of immunotherapy forchronic myelogenous leukemia(CML). CML is a type of cancer in which the bone marrow produces too many red blood cells. This is caused bychromosomal translocation,a mutation in which the abnormal gene BCR-ABL, is turned into a CML cell. CML starts off as amyeloproliferativefor example insickle cell anemiaor extremegranulocytosisbut if left untreated, it could transform into an acute form of leukemia. In order to treat CML, alpha and beta interferons (INFs) are used to regulate the process of binding the protein ICSBP to the gene BCR-ABL. CCL9 was proved to be a gene induced by ICSBP and IFN alpha and also a requirement in the expression of ICSBP in BCR-ABL transformed cells to generate an anti-leukemic immune protection via experimentation. CCL6 and CCL9 were overexpressed in BaF3 cells and injected with BCR-ABL into syngeneic mice. Although the mice still developed leukemia, it delayed the advancement of the disease by several weeks proving that CCL6 and CCL9 contribute to the creation of an anti-leukemic response within infected cells.[6][unreliable medical source]
References[edit]
- ^"Human PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^Zhao X, Sato A, Dela Cruz C, Linehan M, Luegering A, Kucharzik T, Shirakawa A, Marquez G, Farber J, Williams I, Iwasaki A (2003)."CCL9 is secreted by the follicle-associated epithelium and recruits dome region Peyer's patch CD11b+ dendritic cells".J Immunol.171(6): 2797–803.doi:10.4049/jimmunol.171.6.2797.PMID12960300.
- ^Lean J, Murphy C, Fuller K, Chambers T (2002). "CCL9/MIP-1gamma and its receptor CCR1 are the major chemokine ligand/receptor species expressed by osteoclasts".J Cell Biochem.87(4): 386–93.doi:10.1002/jcb.10319.PMID12397598.S2CID23954377.
- ^Youn B, Jang I, Broxmeyer H, Cooper S, Jenkins N, Gilbert D, Copeland N, Elick T, Fraser M, Kwon B (1995)."A novel chemokine, macrophage inflammatory protein-related protein-2, inhibits colony formation of bone marrow myeloid progenitors".J Immunol.155(5): 2661–7.doi:10.4049/jimmunol.155.5.2661.PMID7650394.
- ^abHara T, Bacon K, Cho L, Yoshimura A, Morikawa Y, Copeland N, Gilbert D, Jenkins N, Schall T, Miyajima A (1995)."Molecular cloning and functional characterization of a novel member of the C-C chemokine family".J Immunol.155(11): 5352–8.doi:10.4049/jimmunol.155.11.5352.PMID7594550.
- ^Nardi V, Naveiras O, Azam M, Daley GQ (April 2009)."ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines".Blood.113(16): 3813–20.doi:10.1182/blood-2008-07-167189.PMC2670796.PMID19171873.
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