ITIM-Containing Receptor LAIR1 Inhibits Immune Response and Is Key to Development of Acute Myeloid Leukemia (AML); Blockade of This Signaling May Eliminate Leukemia Stem Cells and Lead to Complete Remission in AML Patients, Senior Author Suggests

University of Texas (UT) Southwestern Medical Center scientists have discovered that a certain class of receptors that inhibit the immune response are crucial for the development of acute myeloid leukemia (AML), the most common acute leukemia affecting adults. The researchers found that some receptors containing the immunoreceptor tyrosine-based inhibition motif (ITIM) are important to the development of AML, providing a new target for potential therapies. “We showed that these receptors are expressed by AML cells and that they support the development of AML. Although counterintuitive, this result is consistent with the generally immune-suppressive, and thus tumor-promoting, roles of inhibitory receptors in the immune system,” said Dr. Chengcheng “Alec” Zhang, Associate Professor of Physiology and Developmental Biology, and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. “These findings suggest that blocking ITIM-receptor signaling, in combination with conventional therapies, may represent a novel strategy for AML treatment.” AML is a type of blood and bone marrow cancer in which certain stem cells or progenitor cells fail to properly mature into healthy white blood cells and, instead, become abnormal red cells, called leukemia cells, according to the National Cancer Institute (NCI), part of the National Institutes of Health (NIH). Leukemia cells can build up in the bone marrow and blood so there is less room for healthy white blood cells, red blood cells, and platelets, which can result in infections, anemia, or bleeding. Leukemia cells also can spread outside the blood to other parts of the body, including the central nervous system, skin, and gums, according to the NCI.
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