Allison Ehrlich

Research:

My primary research interests center around the mechanisms by which the environment influences susceptibility to immune-mediated disease.  Environmental factors are associated with the recent rise in type 1 diabetes, an autoimmune disease characterized by the destruction of insulin-producing beta cells.  One potential mechanistic link between environmental factors and T1D is the aryl hydrocarbon receptor (AhR), a transcription factor that can be activated by diverse ligands found in the diet, microbiome, chemical contaminants, and drugs.  My research aims to identify the mechanisms by which AhR activation leads to divergent CD4+ T cell fates, and tests the hypothesis that the interaction between diverse AhR ligands, the host immune system, and the microbiome influences susceptibility to type 1 diabetes

Education and Experience:

• Ph.D., Yale University, 2014
• B.S., Northeastern University, 2007

Specialties/Focus:

• Immunotoxicology
• Aryl hydrocarbon receptor
• T cell differentiation
• Host-microbiome interactions
• Type 1 diabetes

Teaching:

• ETX 30 - Chemical and Drug Use and Abuse
• ETX 260 - Immunotoxicology

Recent Publications:

Ehrlich AK, Pennington JM, Bisson WH, Kolluri SK, Kerkvliet NI (2018). TCDD, FICZ, and other high affinity AhR ligands dose-dependently determine the fate of CD4+ T cell differentiation. Tox Sci, 161(2):310-320.

Ehrlich AK, Kerkvliet, NI (2017). Is chronic AhR activation by rapidly metabolized ligands safe for the treatment of immune-mediated diseases? Curr Opin Toxicol 2:72-78.

Ehrlich AK, Pennington JM, Tilton S, Wang X, Marshall NB, Rohlman D, Funatake C, Punj S, ODonnel E, Yu Z, Kolluri SK, Kerkvliet NI (2017). AhR activation increases IL-2 production by alloreactive CD4+ T cells initiating the differentiation of mucosal-homing Tim3+Lag3+ Tr1 cells. Eur J Immunol. 11(1981-2001).

Ehrlich AK, Pennington JM, Wang X, Rohlman D, Punj S, Lohr CV, Newman MT, Kolluri SK, Kerkvliet NI (2016). Activation of the aryl hydrocarbon receptor by 10-Cl-BBQ prevents insulitis and effector T cell development independently of Foxp3+ regulatory T cells in nonobese diabetic mice. J Immunol. 196(1):264-73.