CD24: from a Hematopoietic Differentiation Antigen to a Genetic Risk Factor for Multiple Autoimmune Diseases.

Abstract

The autoantibody is an essential characteristic of inflammatory disorders, including autoimmune diseases. Although the exact pathogenic mechanisms of these diseases remain elusive, accumulated evidence has implicated that genetic factors play important roles in autoimmune inflammation. Among these factors, CD24 was first identified as a heat-stable antigen in 1978 and first successfully cloned in 1990. Thereafter, its functional roles have been intensively investigated in various human diseases, especially autoimmune diseases and cancers. It is currently known that CD24 serves as a costimulatory factor of T cells that regulate their homeostasis and proliferation, while in B cells, CD24 is functionally involved in cell activation and differentiation. CD24 can enhance autoimmune diseases in terms of its protective role in the clonal deletion of autoreactive thymocytes. Furthermore, CD24 deficiency has been linked to mouse experimental autoimmune encephalomyelitis. Finally, CD24 genetic variants, including single-nucleotide polymorphisms and deletions, are etiologically relevant to autoimmune diseases, such as multiple sclerosis and systemic lupus erythematosus. Therefore, CD24 is a promising biomarker and novel therapeutic target for autoimmune diseases.

• Authors: Yixin Tan, Ming Zhao, Bo Xiang, Christopher Chang, Qianjin Lu
• Journal: Clinical reviews in allergy & immunology (Clin Rev Allergy Immunol) Vol. 50 Issue 1 Pg. 70-83 (Feb 2016) ISSN: 1559-0267 [Electronic] United States
• PMID: 25666875 (Publication Type: Journal Article, Review)

Chemical References

• CD24 Antigen
• Ligands

Topics

• Animals
• Antigen-Presenting Cells (immunology, metabolism)
• Autoimmune Diseases (diagnosis, drug therapy, etiology, metabolism)
• B-Lymphocytes (cytology, immunology, metabolism)
• CD24 Antigen (chemistry, genetics, metabolism)
• Cell Differentiation
• Clonal Selection, Antigen-Mediated
• Disease Susceptibility
• Gene Expression
• Genetic Predisposition to Disease
• Glycosylation
• Humans
• Ligands
• Lymphocyte Activation
• Molecular Targeted Therapy
• Neoplasms (etiology, metabolism)
• Organ Specificity
• Risk Factors
• Signal Transduction
• T-Lymphocyte Subsets (cytology, immunology, metabolism)