Macrophage inflammatory protein
From Wikipedia, the free encyclopedia
Macrophage Inflammatory Proteins (MIP) belong to the family of chemotactic cytokines known as chemokines. Macrophage inflammatory protein-1 (MIP-1), MIP-1 alpha CCL3 and MIP-1 beta CCL4 are chemokines crucial for immune responses towards infection and inflammation.[3] In humans, there are two major forms, MIP-1α and MIP-1β that are now officially named (CCL3) and (CCL4) respectively. Both are major factors produced by macrophages after they are stimulated with bacterial endotoxins.[4] They activate human granulocytes (neutrophils, eosinophils and basophils) which can lead to acute neutrophilic inflammation. They also induce the synthesis and release of other pro-inflammatory cytokines such as interleukin 1 (IL-1), IL-6 and TNF-α from fibroblasts and macrophages. The genes for CCL3 and CCL4 are both located on human chromosome 17.[5]
They are produced by many cells, particularly macrophages, dendritic cells, and lymphocytes.[6] MIP-1 are best known for their chemotactic and proinflammatory effects but can also promote homoeostasis.[6] Biophysical analyses and mathematical modelling has shown that MIP-1 reversibly forms a polydisperse distribution of rod-shaped polymers in solution. Polymerization buries receptor-binding sites of MIP-1, thus depolymerization mutations enhance MIP-1 to arrest monocytes onto activated human endothelium.[3]
[edit] See also
[edit] References
- ^ Czaplewski, L. G.; McKeating, J.; Craven, C. J.; Higgins, L. D.; Appay, V.; Brown, A.; Dudgeon, T.; Howard, L. A. et al (1999). "Identification of amino acid residues critical for aggregation of human CC chemokines macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES. Characterization of active disaggregated chemokine variants". The Journal of biological chemistry 274 (23): 16077–16084. PMID 10347159. edit
- ^ Lodi, P. J.; Garrett, D. S.; Kuszewski, J.; Tsang, M. L.; Weatherbee, J. A.; Leonard, W. J.; Gronenborn, A. M.; Clore, G. M. (1994). "High-resolution solution structure of the beta chemokine hMIP-1 beta by multidimensional NMR". Science 263 (5154): 1762–1767. PMID 8134838. edit
- ^ a b Ren M, Guo Q, Guo L, et al. (December 2010). "Polymerization of MIP-1 chemokine (CCL3 and CCL4) and clearance of MIP-1 by insulin-degrading enzyme". EMBO J. 29 (23): 3952–66. doi:10.1038/emboj.2010.256. PMID 20959807.
- ^ Sherry B, Tekamp-Olson P, Gallegos C, Bauer D, Davatelis G, Wolpe SD, Masiarz F, Coit D, Cerami A (December 1988). "Resolution of the two components of macrophage inflammatory protein 1, and cloning and characterization of one of those components, macrophage inflammatory protein 1 beta". J. Exp. Med. 168 (6): 2251–9. doi:10.1084/jem.168.6.2251. PMC 2189160. PMID 3058856. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2189160.
- ^ Irving SG, Zipfel PF, Balke J, McBride OW, Morton CC, Burd PR, Siebenlist U, Kelly K (June 1990). "Two inflammatory mediator cytokine genes are closely linked and variably amplified on chromosome 17q". Nucleic Acids Res. 18 (11): 3261–70. doi:10.1093/nar/18.11.3261. PMC 330932. PMID 1972563. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=330932.
- ^ a b Maurer M, von Stebut E (October 2004). "Macrophage inflammatory protein-1". Int. J. Biochem. Cell Biol. 36 (10): 1882–6. doi:10.1016/j.biocel.2003.10.019. PMID 15203102.
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IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16, IFNA17, IFNA21, IFNB1, IFNK, IFNW1
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