My lab is focused on a specific family of proteins called E proteins, which are decision makers that control genetic information and decide what kinds of cells are made. We want to understand how these lineage decisions are made and what the implications of these decisions are in human health. We know that E proteins are important for making B cells and T cells, which are two types of immune cells, but how this process works is poorly understood.

We investigate how this complex process works by studying mice without E proteins. We look at the thymus, a small organ at the top of the chest that trains the immune system to recognize what is normal. Hematopoiesis is a developmental process where hematopoietic stem cells differentiate into different cell types, largely orchestrated by precise transcriptional programs. The basic helix-loop-helix family of transcriptional regulators includes E proteins encoded by the E2A, HEB and E2-2 genes and their inhibitors called Id proteins (Id1-4). Id proteins dimerize with E proteins and inhibit the DNA-binding activity of E proteins. Therefore, the net E protein activity in a cell is determined by the concentration of both E and Id proteins. Research has shown that these proteins play important roles in several steps in hematopoiesis.

Recently, we have found that E proteins play crucial roles in suppressing the innate lymphoid fates while ensuring the robust production of B and T cells. Innate lymphoid cells are newly discovered classes of immune cells implicated in a variety of ailments such as asthma and inflammatory bowel diseases. We are interested in understanding how alternations in E protein function regulates the production of these cells, thus affecting the disease activities. The animal models we have collected over the years also offer us excellent opportunities to study the impact of these cells on immunity as well as tumor microenvironments.