Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related death in the world [1]. Currently, the increasing global disease burden caused by CRC has become one of the major public health problems, due to the growth and aging of the worldwide population. CRC is a multifactorial disease resulting from environmental, lifestyle and genetic factors [2], [3]. However, Most CRCs are arising from precursor lesions such as adenomatous polyps or sessile serrated lesions. The sequential progression of sessile serrated adenomas/polyps through dysplasia from low-grade to high-grade was paired with increasing density of intraepithelial lymphocytes [4], [5]. This growth was a stepwise accumulative process involving a series of histological, morphological, and genetic alterations that generally takes several years or even a decade [2], [6]. However, the immune system’s failure to detect and eradicate tumor cells due to immune surveillance evasion, allows cancer to develop and spread [7], [8], [9].

Over the past decades, it has been shown that immunosurveillance plays a pivotal role in CRC by protecting the host against tumor development and progression [10], [11]. Lymphocyte subpopulations can be divided into three subsets: T cells (CD4+ and CD8+ T cells), B cells and NK cells. They are closely associated with immune responses to tumor cells and the development of solid tumors due to the diverse roles in immune responses [10]. Research has shown that higher lymphocyte infiltration is associated with better outcomes [12]. It has long been known that the presence of brisk T cells infiltrates is correlated with better patient prognosis in a number of human malignancies, for examples, CRC and ovarian cancer [13], [14], [15]. CD4+ T cell subsets were important part of the adaptive immune system. They can secrete interferon (IFN)-γ, activate other lymphocyte subsets by release T cell cytokines and regulate antitumor immune response by directly killing tumor cells [10]. Natural killer (NK) cells are part of the innate immune system. Many studies have demonstrated that NK cells can exert antitumor cell cytotoxicity by monitoring cell surfaces of autologous cells in the absence of antibodies or major histocompatibility complex (MHC) class I molecules [10], [16].

In general, the cancer immunity is a combination of the systemic immune response in circulating peripheral blood and the local immune response in the tumor microenvironment [3]. Most studies focus on local immune response. However, the correlation between the peripheral blood immunity with the tumor development was uncertainty [17]. Using lymphocyte subpopulations infiltrating in tumor tissue for malignancy evaluation of tumors has some limitations because it is neither easily accessible nor dynamically monitored in patients. Therefore, changes in the number, distribution, or functional status of lymphocyte subpopulations in peripheral blood may affect tumor outcomes. In this investigation, we would like to reveal the relationships between lymphocyte subpopulations in the peripheral blood with benign polyps, precancerous polyps and CRC.