Shaodong Dai, PhD

Special Interests

Research Interests

Metal ions are essential nutrients in all forms of life. Despite their important roles, metals can be toxic and elicit different kinds of immune responses, causing diseases. Chronic beryllium disease is a fibrotic lung disorder caused by beryllium exposure, while nickel ion is the dominant allergen for contact dermatitis.

Our major goal is to understand the mechanisms of the metal containing ligands for alpha/beta TCRs from metal reactive human T cells. Using structural biology we will be able to discern the respective rule for metal binding and find potent compounds to inhibit metal binding, thus abrogating T cell responses. We are also interested in the molecular basis of metal induced autoimmunity.

Recently we observed metal ions directly attenuate the binding affinity between TCR and pMHC interaction. Our goal is to understand how the metal ions attenuate the TCR/pMHC binding affinity and what effects they have on T cells activation. The results can help to elucidate the molecular basis for some autoimmunity caused by metals. We are interested in redox signaling in chloroplast and T Cells.

We are studying a unique iron-sulfur enzyme, ferredoxin: thioredoxin reductase, containing both a catalytic [4Fe-4S] cluster and a redox active disulfide. The overall objective of this proposal is to decipher the mechanisms of reduction of disulfide catalyzed by iron sulfur cluster and thiol-disulfide exchange reactions in ferredoxin /thioredoxin system. Redox signaling in apoptosis involves the oxidation and reduction of cysteine residues in critical thiol proteins. Changes in the structure and activity of these proteins can initiate cell responses, or modify the response of cells to other signals.

My proposed research focuses on the regulatory mechanisms of apoptosis signal-regulating kinase 1 (ASK1) mediated T cell apoptosis. ASK1 is a member of the mitogen-activated protein kinase kinase kinase (MAP3K) family, which activates both the SEK1-JNK and MKK3/6-p38 MAP signaling cascades and constitutes a pivotal signaling pathway in cytokine- and stress-induced apoptosis. This signaling pathway mediates a variety of cellular events, including cell proliferation, differentiation, and death.