Seung-Chul Choi, PhD: Research Assistant Scientist


I focus to address the understanding of autoreactive follicular helper T (TFH) cells and effort to regulate excessively generating TFH cells in SLE. I also interest follicular regulatory T (TFR) cell that specifically controls germinal center responses by suppressing TFH and germinal center B cells.

Our lab has previously shown that the differential expression of a novel splice isoform, Pbx1-d, of the Pbx1 gene was associated with the production of autoreactive CD4+ T cells in the Sle1a1 lupus susceptibility locus and lupus susceptibility in the B6.Sle1.Sle2.Sle3 (B6.TC) mouse model. Currently, we have generated B6.CD4-Pbx1-d Tg (Pbx1-d Tg) mice, which specifically express Pbx1-d in CD4+ T cells, and I am studying the mechanisms by which Pbx1 regulates Treg homeostasis and TFH cell differentiation in the Pbx1-d Tg mice, as well as its role in autoimmune pathology in the B6.TC mice. Another interesting study is the autoreactive CD4+ T cell metabolism that is an important checkpoint for CD4+ T cell activation, proliferation, and differentiation. The goal of this study is targeting CD4+ T cell metabolism may abrogate CD4+ T cell inflammatory functions and reduce disease symptoms in SLE mice. Our results have been reported that CD4+ T cells from lupus patients and lupus-prone mice present an elevated glucose metabolism, and that metabolic inhibitors normalized lupus T cell functions in vitro and reversed disease in mice. Remarkably, inhibiting glucose metabolism greatly reduced the frequency of TFH cells in lupus-prone mouse models, and eliminated autoantibodies. Current study is focused on the difference of metabolic demands between spontaneous and exogenous antigen-specific TFH cells. In addition, we also investigate the contribution of the gut microbiota to the therapeutic use of metabolic inhibitors, and our results suggest that regulation of microbiota has a therapeutic effect in SLE disease activity.