CD52

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

CD52
Identifiers
AliasesCD52, CDW52, CD52 molecule, EDDM5, HE5
External IDsOMIM: 114280 HomoloGene: 88652 GeneCards: CD52
Gene location (Human)
Chr.Chromosome 1 (human)[1]
Band1p36.11Start26,317,958 bp[1]
End26,320,523 bp[1]
Orthologs
SpeciesHumanMouse
Entrez

1043

n/a

Ensembl

ENSG00000169442

n/a

UniProt

P31358

n/a

RefSeq (mRNA)

NM_001803

n/a

RefSeq (protein)

NP_001794

n/a

Location (UCSC)Chr 1: 26.32 – 26.32 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human

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[3] and dendritic cells.[4] 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.[5]

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.[6]

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.[7] 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. .[8]

References
  1. GRCh38: Ensembl release 89: ENSG00000169442 - Ensembl, May 2017
  2. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. 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. PMID 12176892.
  4. 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.
  5. 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. ISBN 978-1-59259-076-6. PMID 21337094.
  6. 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.
  7. 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. S2CID 5736696.
  8. 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. S2CID 15841906. Retrieved 28 December 2012.


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