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Calreticulin arms NK cells against leukemia
Jitka Fucikova1,2, Justin P Kline3,4,5, Lorenzo Galluzzi6,7,8,9
1Sotio, Prague, Czech Republic.
Oncoimmunology
|February 1, 2020
Summary
Calreticulin (CALR) on dying cancer cells signals for immune attack. Spontaneous CALR exposure on leukemia also boosts innate immunity through myeloid cells and natural killer (NK) cells.
Area of Science:
- Immunology
- Cancer Biology
- Cellular Signaling
Background:
- Calreticulin (CALR) on the surface of dying cancer cells promotes adaptive anticancer immunity.
- Previous research indicates CALR exposure on cancer cells is a key signal for immune cell recognition and clearance.
Purpose of the Study:
- To investigate the role of spontaneous calreticulin exposure on leukemic cells in innate anticancer immunity.
- To elucidate the mechanism by which CALR influences natural killer (NK) cell-mediated immunity in leukemia.
Main Methods:
- Analysis of calreticulin exposure on leukemic blasts.
- Investigating the interaction between CALR-exposing cells and myeloid CD11c+CD14+ cells.
- Assessing the impact on natural killer (NK) cell activity.
Main Results:
- Spontaneous calreticulin exposure was observed on leukemic blasts.
- This exposure was found to support innate anticancer immunity mediated by natural killer (NK) cells.
- The mechanism involves an indirect pathway dependent on myeloid CD11c+CD14+ cells.
Conclusions:
- Spontaneous calreticulin exposure on leukemia cells contributes to innate anticancer immunity.
- Myeloid CD11c+CD14+ cells act as intermediaries in CALR-mediated NK cell activation.
- Targeting CALR exposure could enhance NK cell-based immunotherapies for leukemia.
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