Start Date
2018
Description
Multiple sclerosis (MS) is an autoimmune disease of the CNS that leads to physical disability, cognitive impairment, and other symptoms associated with neurological damage. MS is a T-cell mediated demyelinating disease with a male to female ratio of 1:3. The molecular mechanisms of sex differences in MS are not well understood. This sexual dimorphism is reflected in experimental autoimmune encephalomyelitis (EAE), a murine model of MS in SJL/J mice. Previous studies show sex-specific differences in immune production and response to IL-33 which promotes a protective Th2 response to EAE in male mice. We set out to understand how sexspecific cell responses to IL-33 affect expression of its receptor, ST2. While many cells express ST2, we focused on mast cells (MCs) as they can respond to and produce IL-33. Bone marrowderived MCs from SJL/J mice were stimulated with IL-33 and expression of ST2 at the RNA and protein levels were assessed. After 24hrs of IL-33 stimulation in early cultures, membrane-bound ST2 expression was higher in male cells and a soluble form of ST2 was lower in male than female cells. This data supports that IL-33 stimulation may trigger a protective autocrine loop that has potential for therapeutic intervention.
Recommended Citation
Tissue, Madison; Gensamer, Rachel; Brown, Melissa; and Caulfield, Margaret, "Sex Differences in Bone Marrow Mast Cell ST2 Expression in Response to IL-33 Stimulation" (2018). Summer Research. 19.
https://digitalcommons.calvin.edu/summer_research/2018/Posters/19
Included in
Sex Differences in Bone Marrow Mast Cell ST2 Expression in Response to IL-33 Stimulation
Multiple sclerosis (MS) is an autoimmune disease of the CNS that leads to physical disability, cognitive impairment, and other symptoms associated with neurological damage. MS is a T-cell mediated demyelinating disease with a male to female ratio of 1:3. The molecular mechanisms of sex differences in MS are not well understood. This sexual dimorphism is reflected in experimental autoimmune encephalomyelitis (EAE), a murine model of MS in SJL/J mice. Previous studies show sex-specific differences in immune production and response to IL-33 which promotes a protective Th2 response to EAE in male mice. We set out to understand how sexspecific cell responses to IL-33 affect expression of its receptor, ST2. While many cells express ST2, we focused on mast cells (MCs) as they can respond to and produce IL-33. Bone marrowderived MCs from SJL/J mice were stimulated with IL-33 and expression of ST2 at the RNA and protein levels were assessed. After 24hrs of IL-33 stimulation in early cultures, membrane-bound ST2 expression was higher in male cells and a soluble form of ST2 was lower in male than female cells. This data supports that IL-33 stimulation may trigger a protective autocrine loop that has potential for therapeutic intervention.