TIM-3 expression may play a critical role in the immune system error experienced by patients with HR-MDS and AML1,2

TIM-3 is a regulator of both innate and adaptive immunity in patients with myeloid diseases.3

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TIM-3 is expressed on multiple immune cell types, including T cells, natural killer cells, macrophages, and DCs

 

TIM-3 expression on immune cells promotes the immune dysfunction associated with disease complexity4

For instance, macrophages have increased TIM-3 expression and do not release cytokines, thus promoting immune tolerance

 

 

There is an opportunity to address the lack of durable response in myeloid diseases with immuno-therapeutic approaches, such as immuno-myeloid therapy, by focusing on TIM-3

 

 

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

 
References: 1. Anderson AC, Joller N, Kuchroo VK. Lag-3, Tim-3, and TIGIT: Co-inhibitory receptors with specialized functions in immune regulation. Immunity. 2016;44(5):989-1004. 2. 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. 3. Das M, Zhu C, Kuchroo V. Tim-3 and its role in regulating anti-tumor immunity. Immunol Rev. 2017;276(1):97-111. 4. Ocaña-Guzman R, Torre-Bouscoulet L, Sada-Ovalle I. TIM-3 regulates distinct functions in macrophages. Front Immunol. 2016;7;1-9.

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