The JC virus (JCV) is a polyomavirus that infects about 75% of the population and encodes the oncogenic T antigen (T-Ag) gene, which inactivates the p53 and pRb/p107/p130 protein families. T-Ag has been found in colorectal neoplasms in previous research conducted in the researcher’s lab. While the majority of persons infected with JCV stay latent, the researchers postulated that a disruption in immune regulation could allow JCV to reactivate, which could play a role in the development of colorectal neoplasia. For a study, the researchers sought to determine if the cell-mediated immune response to JCV T-Ag differed in patients with colorectal adenomatous polyps (AP) or malignancies (CRC). A peptide library covering the full T-Ag protein of JCV activated peripheral blood mononuclear cells (PBMCs) obtained from the blood of patients having a colonoscopy or colorectal surgery. Following T-Ag stimulation, Luminex and flow cytometry tests were used to assess cytokine production and T cell proliferation. In all three groups, JCV T-Ag peptides enhanced IL-2 release, which resulted in T cell growth. Patients without colorectal neoplasms, on the other hand, produced more IL-10 and IL-13. IP-10 was created at extremely high levels in all groups, although there was no statistically significant difference between them. In response to T-Ag cluster activation, the majority of patients had CD4+ and CD8+ T cells. The existence of T-Ag-specific Th1 cells was indicated by the combination of IL-2 and IP-10 secretion in all patients, with the presence of T-Ag-specific Th1 cells being higher in patients without cancer.