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Updated: Jun 22, 2026
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Use of Animal Model of Sepsis to Evaluate Novel Herbal Therapies
Published on: April 11, 2012
Comment on "ALK is a therapeutic target for lethal sepsis"
Rafael B Blasco1, Enrico Patrucco2, Ines Mota2
1Department of Pathology, Children's Hospital Boston and Harvard Medical School, Boston, MA 02115 USA.
Science Translational Medicine
|December 14, 2018
Summary
Anaplastic lymphoma kinase (ALK) is not present in monocytes and macrophages. Therefore, the impact of compounds on stimulator of interferon genes (STING) activation is likely independent of ALK.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase implicated in various cellular processes.
- Stimulator of interferon genes (STING) is a critical mediator of innate immune responses to cytosolic DNA.
- The role of ALK in immune cell function, particularly in monocytes and macrophages, remains incompletely understood.
Purpose of the Study:
- To investigate the expression of anaplastic lymphoma kinase (ALK) in human and mouse monocytes and macrophages.
- To determine if ALK expression is a prerequisite for the effects of bioactive compounds on stimulator of interferon genes (STING) activation.
Main Methods:
- Utilized techniques such as flow cytometry and immunohistochemistry to assess ALK protein expression in monocytes and macrophages.
- Investigated the functional consequences of STING activation in the presence or absence of ALK signaling.
Main Results:
- Physiologically relevant anaplastic lymphoma kinase (ALK) expression was not detected in human and mouse monocytes and macrophages.
- The findings suggest that the activation of stimulator of interferon genes (STING) by bioactive compounds does not rely on the presence of ALK.
Conclusions:
- Anaplastic lymphoma kinase (ALK) is not expressed in key innate immune cells, namely monocytes and macrophages.
- The mechanism of action for compounds modulating STING activation in these cells is likely independent of ALK signaling pathways.
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