I am an immunologist focused on how endocrine signaling contributes to immune responses. Receptors for steroid hormones (estrogens, androgens, and progesterone) are broadly expressed and regulate gene transcription in target cells. We study how these pathways operate in immune cells, particularly how they contribute to the balance between immune homeostasis and chronic inflammation & autoimmunity. Particular areas of interest include mucosal tissues (i.e., intestinal mucosa) and maternal-fetal interface tissues (decidua). Our approach utilizes both preclinical mouse models and primary human cells/tissues.
We are interested in mechanisms by which endocrine hormones influence the immune response. Receptors for steroid hormones (estrogens, androgens, and progesterone) are broadly expressed and regulate gene transcription in target cells. We study how these pathways operate in immune cells, particularly how they contribute to the balance between immune homeostasis and chronic inflammation & autoimmunity.
My lab is focused on the cellular and molecular regulation of mucosal immune responses. I have a particular interest in the non-classical roles of steroid sex hormones (i.e. estrogens, progestins, and androgens) in modulating adaptive and innate immune responses. Signaling via steroid hormones is a critical mechanism of transcriptional regulation in target cells and contributes to homeostatic immune regulation, as well as sexual dimorphism in immune responses.
A major area of research in my laboratory is the role of hormone signaling in the GI tract, and how this shapes innate and adaptive responses in the gut. Our prior work has established novel roles for estrogen-mediated immune protection in both T cells as well as the intestinal epithelium. In addition, we have identified mechanisms by which alterations to these signaling pathways contribute to chronic inflammation in the gut, as in inflammatory bowel disease. We use complementary ex vivo, in vivo, and translational approaches to interrogate the role of estrogen signaling in lymphocytes and epithelial cells from IBD patients and mouse models (Goodman and Garg et al., Mucosal Immunol 2014; Goodman et al., CMGH 2017; Goodman et al., PNAS 2020; Goodman et al., Nat Rev Gastro 2020; etc). Related interests include other paracrine signaling pathways influencing mucosal immunity, including cytokine/chemokine and growth factor signaling. In particular, we are interested in how local environmental cues shape the balance between protective and pathogenic immune responses in the gut, including, but not limited to, T cell differentiation and function; regulatory T cell responses; and immune cell/epithelial crosstalk. This project is supported by an NIH/NIDDK R01, as well as past funding from NIDDK (K01, R03) and the Crohn's & Colitis Foundation.
We are also interested in the immune landscape of pregnancy, focused on the development and maintenance of immune tolerance to the semi-allogenic fetus. We are actively investigating mechanisms by which reproductive hormones influence immune cell differentiation and function at the maternal-fetal interface, and have a particular interest in estrogen/progesterone crosstalk in this process. This project is supported by the March of Dimes Ohio Collaborative, in collaboration with researchers at Cincinnati Children's Medical Center.
- Role of estrogen in modulating intestinal T cell differentiation and function
- Role of estrogen in the intestinal epithelium
- Hormone-mediated control of myeloid cell responses, including macrophages and DCs
- Estrogen/progesterone crosstalk during pregnancy
NIH/NIDDK R01 (2021-2026)
March of Dimes Ohio Collaborative (2020-current)
Crohn's & Colitis Foundation Senior Research Award (2020-2023)
NIH/NIDDK R03 (2020-2023)
NIH/NIDDK K01 (2015-2020)
Crohn's & Colitis Foundation Career Development Award (2015-2018)