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Updated: Aug 11, 2025
Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
Crosstalk between ILC2s and Th2 cells varies among mouse models.
Rama K Gurram1, Danping Wei2, Qiao Yu3
1Molecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Type 2 immune responses involve T helper (Th2) cells and group 2 innate lymphoid cells (ILC2s). These cells collaborate differently depending on the trigger, with Th2 cells expanding ILC2s during helminth infection.
Area of Science:
- Immunology
- Cell Biology
Background:
- Type 2 helper (Th2) cells and group 2 innate lymphoid cells (ILC2s) are crucial for immunity against helminths and allergic reactions.
- The precise roles and interactions between Th2 cells and ILC2s in type 2 immunity remain unclear.
Purpose of the Study:
- To investigate the distinct and collaborative functions of Th2 cells and ILC2s in type 2 immune responses.
- To elucidate the mechanisms underlying Th2 cell and ILC2 activation and crosstalk.
Main Methods:
- Utilized genetically modified mouse models deficient in either ILC2s or Th2 cells.
- Examined immune responses to helminth infection and specific antigen challenges (papain and ovalbumin/alum).
Main Results:
- Interleukin-33 (IL-33) mediated ILC2 activation enhanced Th2 cell responses to papain.
- Thymic stromal lymphopoietin (TSLP) dependent Th2 responses to ovalbumin/alum were independent of ILC2s.
- During helminth infection, Th2 cells induce alarmins (IL-25, IL-33, TSLP), which promote ILC2 expansion, indicating a collaborative immune strategy.
Conclusions:
- Th2 cell differentiation can proceed without ILC2s, but ILC2 activation may bolster Th2 responses.
- Th2 cells play a role in expanding ILC2 populations by inducing type 2 alarmins, highlighting a bidirectional crosstalk in type 2 immunity.
