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Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
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JNK1 negatively controls antifungal innate immunity by suppressing CD23 expression
Xueqiang Zhao1, Yahui Guo1, Changying Jiang2
1Institute for Immunology, Tsinghua University School of Medicine, Beijing, China.
Nature Medicine
|January 24, 2017
Summary
JNK1 activation suppresses antifungal immunity. JNK1-deficient mice showed improved survival against Candida albicans, suggesting JNK inhibitors as potential antifungal therapies.
Area of Science:
- Immunology
- Mycology
- Molecular Biology
Background:
- Opportunistic fungal infections pose a significant threat to immunocompromised individuals.
- Existing antifungal drugs face challenges with toxicity and resistance.
- Mechanisms negatively regulating host antifungal immunity are poorly understood.
Purpose of the Study:
- To investigate the role of JNK1 in regulating host immune responses to fungal infections.
- To identify novel therapeutic targets for antifungal treatments.
Main Methods:
- Comparative analysis of JNK1-deficient and wild-type mice infected with Candida albicans.
- Assessment of immune cell responses, including CD23 expression and nitric oxide production.
- Evaluation of JNK inhibitors in preclinical models.
Main Results:
- JNK1 deficiency significantly enhanced survival rates in a mouse model of Candida albicans infection.
- JNK1 deficiency led to increased CD23 (a C-type lectin receptor) induction via NFATc1.
- Blocking CD23 or nitric oxide production abrogated the enhanced antifungal response in JNK1-deficient mice.
- JNK inhibitors demonstrated potent antifungal effects in both mouse and human cells.
Conclusions:
- JNK1 activation suppresses host antifungal immunity.
- CD23 upregulation and subsequent nitric oxide production are critical mediators of JNK1's suppressive effect.
- JNK1 represents a promising therapeutic target for treating fungal infections, including those caused by Candida albicans.
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