Shawn A. Mahmud

Shawn Mahmud


Entering Class:


St. Olaf College
Biology major
B.A., 2001

University of Minnesota
Ph.D., Microbiology, Immunology and Cancer Biology Graduate Program, 2014

Honors and Awards:

  • Ruth L. Kirschstein NRSA Individual Predoctoral MD/PhD Fellowship (National Institute of Diabetes and Digestive and Kidney Diseases), 2012-2015
  • University of Minnesota Foundation J. Thomas Livermore and Veneziale-Steer Awards, 2014
  • Immunology Training Grant (T32), 2010-2012
  • American Society of Hematology Annual Meeting Travel Award, 2007
  • Microbiology, Immunology, and Cancer Biology Graduate Program Block Fellowship, 2007
  • Crohn’s and Colitis Foundation of America Student Research Fellowship Award, 2007
  • American Society of Hematology Annual Meeting Travel Award, 2006

MSTP Student Governance:

  • Student Advisory Committee 2012-2014

Thesis Advisor: Michael Farrar, Ph.D.

Thesis Research

CD4+ CD25+ Foxp3+ regulatory T cells (Tregs) develop in the thymus and are indispensible for the prevention of systemic autoimmunity by restraining self-reactive T lymphocytes. The mechanism by which developing thymocytes are diverted to the Treg lineage remains unclear, but involves signaling originating from TCR/CD28 and the common gamma chain-dependent cytokine receptor, IL2Rbeta. Signaling through IL2Rbeta activates STAT5 to undergo nuclear translocation where it drives expression of foxp3, the master regulator of the Treg lineage. Transgenic mice expressing constitutively active STAT5 (STAT5b-CA) have a markedly larger Treg population, while STAT5-/- animals show a pronounced deficit. To elucidate the role of STAT5 in driving foxp3 expression, I will utilize BAC recombineering to generate Foxp3-BAC reporter mice with mutated STAT5 binding sites in the promoter and first intron of foxp3, which we predict will negatively regulate Treg development. I will also utilize chromatin immunoprecipitation (ChIP) and bisulfite sequencing techniques to clarify the role of STAT5 in recruiting chromatin-remodeling enzymes to the foxp3 locus which positively regulate its transcription.

By augmenting our understanding of cytokine signaling in the transcriptional control of Treg development, these studies may ultimately contribute to the generation of novel therapeutics for treating autoimmunity or other chronic inflammatory disorders.

Publications (pubmed)

Mahmud SA, Manlove LS, Schmitz HM, Xing Y, Wang Y, Owen DL, Schenkel JM, Boomer JS, Green JM, Yagita H, Chi H, Hogquist KA, Farrar MA. Costimulation via the tumor-necrosis factor receptor superfamily couples TCR signal strength to the thymic differentiation of regulatory T cells. Nat Immunol. 2014 May;15(5):473-81. PMCID: PMC4000541

Mahmud S, Manlove L, Farrar M. Interleukin-2 and STAT5 in regulatory T cell development and function. JAK-STAT Jan 1;2(1):e23154. Review. PMCID: PMC3670270

Vang KB, Yang J, Mahmud SA, Burchill MA, Vegoe AL, Farrar MA. IL-2, -7, and -15, but Not Thymic Stromal Lymphopoeitin, Redundantly Govern CD4+Foxp3+ Regulatory T Cell Development. J Immunol 2008 181: 3285-3290. PMCID: PMC2810104

Publications Prior to Entering MD/PhD Program:

Wang JG, Mahmud SA, Bitterman PB, Huo Y, Slungaard A. Histone deacetylase inhibitors suppress TF-kappaB-dependent agonist-driven tissue factor expression in endothelial cells and monocytes. J Biol Chem. 2007;282:28408-28418.

Kowalska MA, Mahmud SA, Lambert MP, Poncz M, Slungaard A. Endogenous platelet factor 4 stimulates activated protein C generation in vivo and improves survival after thrombin or lipopolysaccharide challenge. Blood. 2007;110:1903-1905.

Wang JG, Mahmud SA, Ngugen J, Slungaard A. Thiocyanate-Dependent Induction of Endothelial Cell Adhesion Molecule Expression by Phagocyte Peroxidases. A Novel HOSCN-Specific Oxidant Mechanism to Amplify Inflammation. J Immunol. 2006;177: 8714-8722.

Wang JG*, Mahmud SA*, Thompson JA, Geng JG, Key NS, Slungaard A. The principal eosinophil peroxidase product, HOSCN, is a uniquely potent phagocyte oxidant inducer of endothelial cell tissue factor activity: a potential mechanism for thrombosis in eosinophilic inflammatory states. Blood 2006;107: 558-565. (*Authors contributed equally to this manuscript)