The Sumida Lab

A primary focus of the Sumida Lab is the study and exploration of the factors and mechanisms that control immune tolerance and dysfunction in human health and disease, with a particular emphasis on the role of regulatory T cells. The lab seeks to better understand the molecular mechanisms that disrupt homeostatic programs of the immune system, with the goal of disease prevention or halting its progress. Accumulating evidence implicate Foxp3⁺ regulatory T cells (Tregs) as being critical to the proper suppression of aberrant activation of autoreactive T cells. In addition, co-stimulatory/inhibitory receptor signaling contribute to fundamental pathways that govern immune cell activation. Thus, dysregulation of Tregs and unbalanced co-stimulatory/inhibitory signals are strongly implicated in immunopathogenesis. Reversing the loss of Treg function and tuning the balance between co-stimulatory/inhibitory signals are potentially therapeutic options for treating autoinflammatory diseases, including multiple sclerosis (MS).

We focus on basic human immunobiology and gene regulatory programs that cause autoinflammatory disease, especially MS. We are studying the interaction of genetics and epigenetics to understand pathogenic gene regulatory circuits in primarily human T cells, with a focus on the functional roles of co-inhibitory receptors. Among human T cells, we are interested in how Foxp3⁺ Tregs play an indispensable role in maintaining immune homeostasis. We think the study of the dynamic balance of pro- and anti-inflammatory signals is necessary to decipher complex dynamic immune response to genetic and environmental factors.