Chronic myelogenous leukemia (CML) is caused by the BCR-ABL chimeric tyrosine kinase, which is derived from the reciprocal translocation, t(9;22)(q34;q11). BCR-ABL tyrosine kinase inhibitors (TKIs) can provide prolonged overall survival in CML patients, resulting in life expectancy nearly to general population, and now approximately half of patients who achieved deep molecular response (DMR) can sustain durable molecular remission after discontinuation TKIs. However, residual leukemic cells still detected in the patients who sustained in molecular remission after discontinuation TKIs with the sensitive BCL-ABL1 transcript detection method. Given the fact that residual leukemic cells can exist in these patients, host immune systems can protect the patients to develop CML progression derived from residual leukemic cells. The human immune system is generally composed by innate and adaptive immune systems, corresponding to their functional diversities. Natural killer (NK) cells are major components of the innate immune system, while T lymphocytes (T cells) are major components of the adaptive immune system, and both NK cell and T cell mediate immune responses have an important role in CML. Myeloid-derived suppressor cells (MDSCs) that promote expansion of regulatory T cells (Tregs), leading to host immune suppression, are also important. Although regulation mechanism of these immune system has not been fully elucidated, tumor antigen (e.g. Wilms tumor-1), and surface receptors (e.g. killer immunoglobulin-like receptor and natural killer group 2) on NK cells, are pivotal role in these immune system regulations. Hence, we reviewed the current the immunological analysis, especially T cell and NK cell immunity in CML.
Keywords: Chronic myelogenous leukemia; Killer immunoglobulin-like receptor; Natural killer cell immunity; T cell immunity; Wilms tumor-1.
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