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RefSeq (mRNA)



RefSeq (protein)



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CAMPATH-1 antigen, also known as cluster of differentiation 52 (CD52), is a glycoprotein that in humans is encoded by the CD52 gene.

CD52 is present on the surface of mature lymphocytes, but not on the stem cells from which these lymphocytes were derived. It also is found on monocytes[1] and dendritic cells.[2] Further, it is found within the male genital tract and is present on the surface of mature sperm cells.

CD52 is a peptide of 12 amino acids, anchored to glycosylphosphatidylinositol (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.[3]

CD52 binds the ITIM (immunoreceptor tyrosine-based inhibitory motif)-bearing sialic acid-binding lectin SIGLEC10.

Clinical significance

It is associated with certain types of lymphoma.[4]

It is the protein targeted by alemtuzumab, a monoclonal antibody used for the treatment of chronic lymphocytic leukemia. A phase III trial into treatment of relapsing-remitting multiple sclerosis showed a reduction in relapse rate, but no statistically significant reduction in accumulated disability, when used as a first-line therapy.[5] However, a sister study looking at patients in whom relapses had occurred despite treatment with interferon beta or glatiramer demonstrated 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. .[6]


  1. 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. PMID 12176892.
  2. 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. PMID 12393688.
  3. 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. PMID 21337094.
  4. 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. PMID 17488672.
  5. 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. PMID 23122650.[unreliable medical source?]
  6. 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. PMID 23122652. Retrieved 28 December 2012.

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