Ptprc, also known as CD45, is a transmembrane glycoprotein. It is an essential regulator of T and B cell antigen receptor-mediated activation, playing a key role in maintaining the equilibrium between protein tyrosine kinase and phosphatase activity. Disruptions can lead to immunodeficiency, autoimmunity, or malignancy. It is expressed on almost all haematopoietic cells except mature erythrocytes and functions upstream of a large signalling network [1].

In cutaneous melanoma, PTPRC is positively correlated with positive prognosis, and its knockdown enhances melanoma cell migration, invasion, and proliferation [2]. In breast cancer, PTPRC promotes CD8+ T cell-mediated tumor immunity and drug sensitivity, and intracellular down-regulation of PTPRC enhances paclitaxel tolerance in triple-negative breast cancer cell lines [3]. In pediatric acute myeloid leukemia, high PTPRC expression is associated with a worse overall survival rate and is an independent adverse prognostic factor, and its expression level is correlated with the infiltration level of activated dendritic cells [5]. In rheumatoid arthritis, the PTPRC rs10919563 A allele shows a poor response to anti-TNF therapy [4]. In HIV-1 seroconverters, PTPRC and interferon-response pathways have significantly higher expression prior to infection [6]. In Parkinson's and progressive supranuclear palsy disorders, PTPRC mRNA is downregulated in PSP patients compared to PD and healthy controls, and it may be useful as part of a biosignature to stratify patients according to disease severity and progression [7].

In conclusion, Ptprc is crucial for the regulation of immune cell functions. Studies on Ptprc in various diseases such as melanoma, breast cancer, leukemia, rheumatoid arthritis, HIV-1 infection, and neurodegenerative disorders have provided insights into its role in disease prognosis, immune cell infiltration, and response to therapy. These findings highlight the importance of Ptprc as a potential biomarker and therapeutic target in multiple disease areas.