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Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
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Group 3 innate lymphocytes (ILC3s) upregulate IL-22 in response to elevated intracellular cAMP levels
Prakash Sah1, Jonathan T Derouen1, Justine L Alexander1
1Department of Microbiology and Immunology, College of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Cytokine
|March 20, 2022
Summary
Bacillus anthracis edema toxin directly activates group 3 innate lymphocytes (ILC3s), enhancing IL-22 production. This contrasts with lethal toxin and suggests a role for cyclic adenosine monophosphate (cAMP) signaling in ILC3 activation.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Group 3 innate lymphocytes (ILC3s) are crucial for mucosal immunity against bacterial pathogens.
- ILC3s are typically activated by cytokines like IL-23 and IL-1β.
- Bacillus anthracis produces toxins that modulate the host immune response.
Purpose of the Study:
- To investigate the effect of Bacillus anthracis edema toxin on ILC3 function.
- To determine if edema toxin activates ILC3s independently of canonical cytokine stimulation.
- To explore the role of cyclic adenosine monophosphate (cAMP) signaling in ILC3 activation.
Main Methods:
- Treatment of a mouse ILC3-like cell line with Bacillus anthracis edema toxin.
- Analysis of IL-22 production following toxin treatment.
- Assessment of CREB phosphorylation and comparison with forskolin treatment.
Main Results:
- Edema toxin directly activated ILC3s, independent of IL-23 or IL-1β.
- Edema toxin upregulated the production of the key effector cytokine IL-22.
- Forskolin treatment mimicked edema toxin's effects and increased CREB phosphorylation, indicating a role for cAMP signaling.
Conclusions:
- Bacillus anthracis edema toxin activates ILC3s, promoting IL-22 production.
- This activation is mediated through cyclic adenosine monophosphate (cAMP) signaling pathways.
- Edema toxin's effect on ILC3s contrasts with lethal toxin's inhibitory function, highlighting differential toxin impacts on innate immunity.
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