Ctla2a, known as cytotoxic T lymphocyte-associated protein 2 alpha, is a tissue-specific secretory factor in mice [1]. It has been associated with multiple biological processes.

Ctla2a is involved in inflammation-related pathways, as indicated by its up-regulation in response to chronic social stress in the hippocampus of mice, where genes related to injury response and inflammation were affected [3]. It is also an immunosuppressive factor, with its down-regulation in P2X4 receptor knockout mice after ischemic stroke, suggesting its role in immune modulatory pathways for cerebroprotection [4,7].

In the study of ruminant trans-fatty acid intake, Ctla2a was among the genes whose expression was altered in the adipose tissue of C57BL/6 mice. TPA intake, compared to EA intake, led to the up-regulation of Ctla2a, and these genes were related to multiple signaling pathways including NOD-like receptor, lipid and atherosclerosis, and inflammatory mediator regulation of TRP channels signaling [2].

In the conversion of Th2 to Th9 cells, Ctla2a was identified among the receptors associated with significant differentially altered genes, suggesting its potential role in the development of various diseases related to Th9 cells [5].

In the acute phase of temporal lobe epilepsy, Ctla2a was identified as one of the Hub genes through combined transcriptomics and proteomics analysis, providing a theoretical basis for adding diagnostic biomarkers for this disease [6].

In conclusion, Ctla2a is a multi-functional gene involved in inflammation, immunosuppression, and various disease-related biological processes. Mouse models, such as those with genetic deletion like P2X4 receptor knockout mice, have been crucial in revealing its role in ischemic stroke cerebroprotection. Its identification in different disease-related gene expression studies, like in temporal lobe epilepsy and the study of Th9 cell-related diseases, further emphasizes its significance in understanding disease mechanisms.