An immuno-myeloid approach focusing on TIM-3 expression may help address the immune dysfunction of HR-MDS and AML.1-5 Watch Dr Komrokji explain.

Immune dysfunction has emerged as a key driver of HR-MDS and AML1-3



TIM-3 may be responsible for immune dysfunction in higher-risk myelodysplastic syndromes and AML4,5



Can addressing immune dysfunction lead to durable responses in patients with HR-MDS and AML?



AML: acute myeloid leukemia; HR-MDS: higher-risk myelodysplastic syndromes; TIM-3: T cell immunoglobulin and mucin domain-3.

References: 1. Lopes MR, Traina F, Campos PdM, et al. IL10 inversely correlates with the percentage of CD8+ cells in MDS patients. Leuk Res. 2013;37(5):541-546. 2. Ma L, Ceuppens J, Kasran A, et al. Immature and mature monocyte-derived dendritic cells in myelodysplastic syndromes of subtypes refractory anemia or refractory anemia with ringed sideroblasts display an altered cytokine profile. Leuk Res. 2007;31(10):1373-1382. 3. Kiladjian J-J, Bourgeois E, Lobe I, et al. Cytolytic function and survival of natural killer cells are severely altered in myelodysplastic syndromes. Leukemia. 2006;20(9):463-470. 4. Monney L, Sabatos CA, Gaglia JL, et al. Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease. Nature. 2002;415(6871):536-541. 5. Kikushige Y, Shima T, Takayanagi S-I, et al. TIM-3 is a promising target to selectively kill acute myeloid leukemia stem cells. Cell Stem Cell. 2010;7(6):708-717.