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Updated: Mar 30, 2026
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Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
Published on: June 27, 2020
5.9K
Androgens protect ILC2S from functional suppression during influenza virus infection
Sapana Kadel1, Reegan A J Miller1, Anna Karlik2
1Arthritis & Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK 73104, USA; Dept. of Microbiology & Immunology, University of Oklahoma Health Campus, 1100 N. Lindsay Ave, Oklahoma City, OK 73104, USA.
Mucosal Immunology
|March 28, 2026
Summary
Androgen receptor (AR) activity in male immune cells preserves function during influenza A virus infection. In females, AR signaling is reduced, leading to immune suppression and impacting influenza A virus outcomes.
Area of Science:
- Immunology
- Virology
- Endocrinology
Background:
- Biological sex influences immune responses to influenza A virus (IAV).
- Females exhibit stronger interferon-centered immune responses, but sex steroid receptor roles in immune cells are unclear.
- Lung-resident group 2 innate lymphoid cells (ILC2s) express androgen receptors (AR) and are crucial for tissue repair post-IAV infection.
Purpose of the Study:
- Investigate sex differences in ILC2 functional suppression during IAV infection.
- Elucidate the role of androgen receptors (AR) in regulating ILC2 function in a sex-specific manner.
- Determine the molecular mechanisms underlying ILC2 sex dimorphism in response to IAV.
Main Methods:
- Comparative analysis of ILC2 function (proliferation, cytokine production, gene expression) between male and female mice during sublethal IAV infection.
- Transcriptomic analysis to identify sex-biased gene expression in ILC2s.
- In vivo studies using lymphocyte-restricted STAT1-deficient and ILC2-restricted AR-deficient mouse models.
- Hormonal manipulation via orchiectomy in male mice.
Main Results:
- Female ILC2s exhibited attenuated proliferation and reduced production of IL-5 and amphiregulin compared to males.
- Female ILC2s showed decreased expression of GATA3 and IL-33R, with elevated IFNGR and phospho-STAT1 levels post-IFNγ stimulation.
- Lymphocyte-restricted STAT1 deficiency reversed IAV-induced suppression of female ILC2s.
- ILC2-restricted AR deficiency increased IFNGR expression, and androgen loss via orchiectomy suppressed male ILC2s.
Conclusions:
- Androgen receptor (AR) activity within ILC2s attenuates IFNGR-STAT1 signaling, preserving ILC2 function in males during IAV infection.
- Sex differences in ILC2 function during IAV infection are driven by intrinsic factors, specifically AR-mediated regulation of interferon signaling.
- These findings highlight a novel mechanism of sex-based immune regulation relevant to viral infections.
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