My research centers on immune regulation of microbe-immune interactions, and how this relationship relates to autoimmune diseases such as inflammatory bowel disease, multiple sclerosis, and systemic lupus erythematosus.
My current research involves characterization of the role regulatory T cells play in shaping immune responses to self-antigens and microbiota antigens of the extended self. My lab is approaching this question through the development of the novel in vitro models of microbe-immune interaction. My previous research has spanned numerous areas including 1) utilization of genetic tools to develop innovative mouse models to study the role of self-antigen and microbiota-driven autoimmunity, 2) the role of vitamin D in autoimmune disease, and 3) B lymphocyte development and genetic dissection of B cell-mediated autoimmunity. In the classroom, I seek to engage and energize my students both by incorporating active learning and student-centered approaches and with an enthusiastic and passionate attitude toward learning. I also enjoy training young scientists in the lab and utilize my research as another opportunity to promote inquiry-based learning.
- Spanier J.A., Nashold F.E., Mayne C.G., Hayes CE. Vitamin D and estrogen synergy in Vdr-expressing CD4+ T cells is essential to induce Helios+FoxP3+ T cells and prevent autoimmune demyelinating disease. J Neuroimmunology. 2015 Sep 15;286:48-58.
- Mayne, C.G., Williams, C.B. Induced and natural regulatory T cells in the development of inflammatory bowel disease. Inflammatory Bowel Diseases. 2013 Jul;19(8):1772-88.
- Mayne C.G., Spanier J.A., Relland L.M., Williams C.B., Hayes C.E. 1,25-Dihydroxyvitamin D3 acts directly on the T lymphocyte vitamin D receptor to inhibit experimental autoimmune encephalomyelitis. Eur J Immunol. 2011 Mar;41(3):822-32.
- Hayes, C.E., Nashold F.E., Mayne C.G., Spanier J.A., and Nelson C.D. 2011. Vitamin D and Multiple Sclerosis. Vitamin D, Third Edition. Ed. by Feldman, Pike and Adams. Acad Press.
- Mayne, C.G., Amanna, I.A., and Hayes C.E. BAFF-Receptor residues 168-175 are essential for optimal CD21 expression but dispensable for B cell survival. Mol Immunol. 2009 Dec;47(2-3):590-9.
- Mayne, C. G., F. E. Nashold, Y. Sasaki, and C. E. Hayes. Altered BAFF-receptor signaling 4nd additional modifier loci contribute to systemic autoimmunity in A/WySnJ mice. Eur J Immunol 2009 39:589-599.
- Mayne, C. G., I. J. Amanna, F. E. Nashold, and C. E. Hayes. Systemic autoimmunity in BAFF-R-mutant A/WySnJ strain mice. Eur J Immunol 2008 38:587-598.