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Updated: Mar 17, 2026

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
Innate B Cells Tell ILC How It's Done
Trang T T Nguyen1, Nicole Baumgarth2
1Center for Comparative Medicine, University of California, Davis, Davis, CA 95616, USA; Graduate Group in Immunology, University of California, Davis, Davis, CA 95616, USA.
Earlier responding innate-like B cells (NKB) were found to induce protective innate lymphoid cell (ILC) responses. This study reveals a novel upstream regulator of ILC function in early immunity.
Area of Science:
- Immunology
- Cellular Biology
- Infectious Disease
Background:
- Innate lymphoid cells (ILCs) are crucial early responders to infection.
- ILCs also play a role in shaping adaptive immune responses, particularly CD4(+) T cell differentiation.
- The upstream regulators of ILC activation and function remain incompletely understood.
Purpose of the Study:
- To investigate the role of innate-like B cells (NKB) in initiating immune responses.
- To determine if NKB cells influence the function of innate lymphoid cells (ILCs).
- To elucidate the sequence of immune cell activation during early host defense.
Main Methods:
- Flow cytometry analysis of immune cell populations in response to infection models.
- In vivo cell depletion and adoptive transfer experiments.
- Cytokine profiling of ILCs and T cells following NKB cell activation.
Main Results:
- Fan and colleagues identified innate-like B cells (NKB) as early responders in infection models.
- NKB cell activation was shown to precede and induce protective innate lymphoid cell (ILC) responses.
- These NKB-induced ILC responses were critical for instructing subsequent CD4(+) T cell cytokine profiles.
Conclusions:
- Innate-like B cells (NKB) represent a previously unrecognized upstream activator of innate lymphoid cells (ILCs).
- NKB cells initiate protective immune responses by priming ILCs early in infection.
- This finding expands our understanding of early immune cell crosstalk and host defense mechanisms.
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