CD52
| CD52 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Aliases | CD52,CDW52, CD52 molecule, EDDM5, HE5 | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM:114280;HomoloGene:88652;GeneCards:CD52;OMA:CD52 - orthologs | ||||||||||||||||||||||||||||||||||||||||||||||||||
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CAMPATH-1 antigen,also known ascluster of differentiation52(CD52), is aglycoproteinthat in humans is encoded by theCD52gene.
CD52 is present on the surface of maturelymphocytes,but not on thestem cellsfrom which these lymphocytes were derived. It also is found onmonocytes[3]anddendritic cells.[4]Further, it is found within the male genital tract and is present on the surface of maturesperm cells.
CD52 is apeptideof 12 amino acids, anchored toglycosylphosphatidylinositol(GPI). Since it is highly negatively charged and present on sperm cells and lymphocytes, it has been conjectured that its function is anti-adhesion, allowing cells to freely move around.[5]
CD52 binds the ITIM (immunoreceptor tyrosine-based inhibitory motif)-bearing sialic acid-binding lectinSIGLEC10.
Clinical significance[edit]
It is associated with certain types oflymphoma.[6]
It is the protein targeted byalemtuzumab,amonoclonal antibodyused for the treatment ofchronic lymphocytic leukemiaandorgan transplantation.A phase III trial into treatment of relapsing-remittingmultiple sclerosisshowed a reduction in relapse rate, but no statistically significant reduction in accumulated disability, when used as a first-line therapy.[7]However, a sister study looking at patients in whom relapses had occurred despite treatment withinterferon betaorglatiramerdemonstrated reduction in both relapse rate and accumulated disability. 20% patients randomised to interferon beta 1a had "sustained accumulation of disability" compared with 13% in the alemtuzumab group.[8]
References[edit]
- ^abcGRCh38: Ensembl release 89: ENSG00000169442–Ensembl,May 2017
- ^"Human PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^Buggins AG, Mufti GJ, Salisbury J, Codd J, Westwood N, Arno M, Fishlock K, Pagliuca A, Devereux S (September 2002)."Peripheral blood but not tissue dendritic cells express CD52 and are depleted by treatment with alemtuzumab".Blood.100(5): 1715–20.doi:10.1182/blood.V100.5.1715.h81702001715_1715_1720.PMID12176892.
- ^Ratzinger G, Reagan JL, Heller G, Busam KJ, Young JW (February 2003)."Differential CD52 expression by distinct myeloid dendritic cell subsets: implications for alemtuzumab activity at the level of antigen presentation in allogeneic graft-host interactions in transplantation".Blood.101(4): 1422–9.doi:10.1182/blood-2002-04-1093.PMID12393688.
- ^Hale G, Waldmann H (2000)."From Laboratory to Clinic: The Story of CAM PA TH-1".Methods Mol. Med.40:243–66.doi:10.1385/1-59259-076-4:243.ISBN978-1-59259-076-6.PMID21337094.
- ^Piccaluga PP, Agostinelli C, Righi S, Zinzani PL, Pileri SA (April 2007)."Expression of CD52 in peripheral T-cell lymphoma".Haematologica.92(4): 566–7.doi:10.3324/haematol.10767.hdl:11585/51398.PMID17488672.
- ^Coles AJ, Twyman CL, Arnold DL, Cohen JA, Confavreux C, Fox EJ, Hartung HP, Havrdova E, Selmaj KW, Weiner HL, Miller T, Fisher E, Sandbrink R, Lake SL, Margolin DH, Oyuela P, Panzara MA, Compston DA (November 2012). "Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial".Lancet.380(9856): 1829–39.doi:10.1016/S0140-6736(12)61768-1.PMID23122650.S2CID5736696.[unreliable medical source?]
- ^Cohen, Jeffrey; Coles A; Arnold D (24 November 2012)."Alemtuzumab versus interferon beta 1a as first-line treatment for patients with relapsing-remitting multiple sclerosis: a randomised controlled phase 3 trial".The Lancet.380(9856): 1819–1828.doi:10.1016/S0140-6736(12)61769-3.PMID23122652.S2CID15841906.Retrieved28 December2012.
External links[edit]
- CD52+antigenat the U.S. National Library of MedicineMedical Subject Headings(MeSH)
- HumanCD52genome location andCD52gene details page in theUCSC Genome Browser.