PubMed Health⌕ Search

PubMed · 11257744

CD52 antigen--a review.

Abstract

Human CD52 is a glycosylphosphatidylinositol (GPI)--anchored antigen expressed on the all lymphocytes as well as within the male genital tract, where it can be produced by epithelial cells of the distal epididymis and duct deferens. CD52 can be shed into seminal plasma and then acquired by sperm cells during their passage through the genital tract, thus it is detectable on the surface of epididymal sperm and in the ejaculate but not on either spermatogenetic cells or testicular spermatozoa. Protein core of the sperm and lymphocyte CD52 is identical and it is a product of a single copy gene located on chromosome 1. However, N-linked carbohydrate side chains (attached to Asn-3) and GPI-anchor structure are different. Physiological role of CD52 on lymphocytes is unclear, although antibody directed to CD52, CAMPATH-1, is capable of complement activation and it can be clinically useful to treat lympho-proliferative disorders and to deplete lymphocytes in bone marrow transplants. Monoclonal antibodies directed against sperm CD52 may cause sperm immobilisation and agglutination and affect hamster oocyte penetration suggesting an association of this molecule with fertilisation.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Domagała, M Kurpisz. CD52 antigen--a review.. https://pubmed.ncbi.nlm.nih.gov/11257744/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Autophagic-like cell death in neutrophils induced by autoantibodies.

Human neutrophils undergo autophagic-like cell death following Sialic acid binding immunoglobulin-like lectin-9 (Siglec-9) ligation and concurrent stimulation with certain, but not all, neutrophil survival cytokines. Caspase inhibition by these cytokines is required, but is not sufficient, to trigger this particular form of cell death. Additional mechanisms may involve reactive oxygen species (ROS), and blocking of ROS or prevention of ROS production prevents autophagic-like neutrophil death. Interestingly, human intravenous immunoglobulin (IVIg) preparations contain natural anti-Siglec-9 autoantibodies, which are able to ligate Siglec-9 on neutrophils and induce autophagic-like cell death in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and some other survival cytokines. Here, we discuss the pathophysiological and therapeutic implications of these recent findings.

Antigens, CD↗

Bias in association studies of systemic lupus erythematosus susceptibility due to geographical variation in the frequency of a programmed cell death 1 polymorphism across Europe.

We obtained eight collections of DNA samples from ethnically matched systemic lupus erythematosus (SLE) patients and controls from five European countries totaling 783 patients and 1210 controls. A highly significant cline in the frequency of the PD1.3 A allele was found among controls but not among SLE patients. The frequency of the PD1.3 A allele increased from the Northeast to the Southwest of Europe. The cline was clearly apparent (P=1.2 x 10(-6)) when data from controls of other five SLE susceptibility studies were included in the analysis. This variation has severely biased SLE association studies owing to the lack of parallel changes in SLE patients. As a consequence, the PD1.3 A allele was more common in SLE patients than in controls in the Northeast and Center of Europe, similar to controls in Southeast Europe, and less frequent than in the controls in the Southwest of the Continent. This dissociation in allele frequencies between SLE patients and controls in different subpopulations indicated that programmed cell death 1 variation and disease susceptibility are not independent but the type of relationship is currently unclear. As allele frequency clines are common in other polymorphisms their impact in genetic epidemiology studies should be carefully considered.

Antigens, CD↗