CD52

Official Full Name

CD52 molecule

Organism

Homo sapiens

GeneID

1043

Background

Involved in positive regulation of cytosolic calcium ion concentration. Predicted to be located in extracellular region and plasma membrane. Predicted to be active in sperm midpiece. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

HE5; CDW52; EDDM5;

Protein Sequence

MKRFLFLLLTISLLVMVQIQTGLSGQNDTSQTSSPSASSNISGGIFLFFVANAIIHLFCFS

Open

Disease

Mature B-cell leukaemia, Multiple sclerosis

Approved Drug

1 +

Clinical Trial Drug

1 +

Discontinued Drug

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Tag	Price

Cat.No.	Product Name	Price

Detailed Information

Mostly expressed on lymphoid cells, including CD4+ T cells and B cells, the CD52 gene generates a small glycosylphosphatidylinositol (GPI)-anchored glycoprotein, which also finds expression in myeloid cells including CD16+ dendritic cells and monocytes. Though discovered as the target of the lymphocyte-depleting monoclonal antibody CAMPATH, the exact physiological roles of CD52 are still unknown. Recent studies, however, have shed light on its possible functions in immunological control as well as its participation in disorders such as lymphoproliferative syndrome and Listeria meningitis.

Gene Function and Pathways

Predicted to be found in the extracellular area and plasma membrane, CD52 is essentially engaged in the positive control of cytosolic calcium ion concentration and is thereby an inherent component of the latter. Although its expression in immune cells is very high and points to a probable function in immune response control, this has not yet been completely identified. Among the many routes connected to CD52 are post-translational modifications including the production of GPI-anchored proteins and protein metabolism.

Specifically in response to microbial compounds and host-derived damage-associated molecular patterns (DAMPs), the gene is evolutionarily conserved and functions in immune system detection. Given the growing research focus on targeting innate immune system signaling pathways for therapeutic uses, CD52 may affect inflammation-driven diseases—which is important.

Biological Functions of CD52

The glycosylation of CD52 is well-known; it consists of a complex N-linked core fucosylated polylactosamine multi-antennary sialylated glycan. For CD52 to be effective, its GPI anchor is vital. The generation of soluble CD52 via phospholipase C cleavage has been shown to bind to the inhibitory receptor Siglec-10, which is increased on activated T cells. This interaction underlines the function of CD52 in immunological control because it is supposed to reduce T cell activation. Still under research, however, are its other possible uses.

Particularly in relation to T-cell activation, CD52 is clearly important for immunological control. Further confirming its possible function in immunological regulation, high expression levels of CD52 on T cells have been associated with the inhibition of bystander T-cell activation. Though the wider consequences of soluble CD52 in other immune responses remain unknown, its interaction with Siglec-10 offers a molecular explanation for this regulating role.

Figure 1 illustrates how CD52 Fc suppresses the production and secretion of inflammatory cytokines. Figure 1. Schematic model showing how CD52 Fc suppresses inflammatory cytokine production and secretion. (Rashidi M, et al., 2018)

CD52 in Cancer and Therapeutic Implications

Studies on possible biomarkers for cancer detection and treatment have increasingly turned to CD52. The expression pattern of CD52 in tumors, including lung cancer, points to possible effects on tumor behavior especially in the tumor microenvironment. The association of tumor-infiltrating lymphocytes with chemotherapy response and patient prognosis emphasizes the need to know how immune-modulating proteins such as CD52 interact with the tumor microenvironment.

Globally, non-small cell lung cancer (NSCLC) in particular ranks as the major cause of illness and death. About 85% of all lung cancer cases are NSCLC-accounted for; its subtypes, squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) are common. Though immunotherapy and targeted therapy have advanced, NSCLC treatment is still difficult mostly because to medication resistance and adverse effects. Improving diagnosis and therapy therefore depends on the identification of novel molecular targets.

Recent research has underlined CD52 as a prognostic marker in breast cancer and its possible function in changing the immune response in other malignancies. Given its function in controlling tumor-infiltrating immune cells, CD52 might be a useful therapeutic target either alone or in concert with other immune checkpoint inhibitors such as PD-1/PD-L1 inhibitors.

Within the framework of NSCLC, CD52 expression has been assessed by immunohistochemical labeling and investigated biologically by loss-of-function experiments both in vitro and in vivo. These investigations seek to ascertain if CD52 fuels the malignant behavior of NSCLC cells and whether its suppression can change the course of a tumor.

CD52 in Autoimmune Diseases

CD52 also plays a role in autoimmune diseases, where it has been targeted by the monoclonal antibody Alemtuzumab. Targeting CD52 offers therapeutic promise as shown by the treatment of multiple sclerosis and chronic lymphocytic leukemia with alemtuzumab. The antibody reduces symptoms of autoimmune illnesses by decreasing cells expressing CD52, hence regulating immune response.

Though much research on CD52 has focused on lymphocyte depletion, its wider influence on the immune system and function in disorders such as Listeria meningitis and lymphoproliferative syndrome point to possible therapeutic uses. Studies on the function of CD52 in autoimmune illnesses and its part in the immune system are growing and expose its potential target for precision treatment.

References:

Rashidi M, Bandala-Sanchez E, Lawlor KE, et al. CD52 inhibits Toll-like receptor activation of NF-κB and triggers apoptosis to suppress inflammation. Cell Death Differ. 2018;25(2):392-405.
Cai Y, Zhao J, Luo C, et al. CD52 knockdown inhibits aerobic glycolysis and malignant behavior of NSCLC cells through AKT signaling pathway. J Cancer. 2024;15(11):3394-3405.

Quick Inquiry

Interested in learning more?

Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.

Request a quote today!

Inquiry