Qing Ching Chen, MD, PhD, is Associate Professor of Pathology at the University of Maryland School of Medicine. She serves as Director of Hematopathology Section, Director of Hematopathology Fellowship Training Program, and Medical Director of the Clinical Flow Cytometry Laboratory. Dr. Chen completed her residency and fellowship training in anatomic/clinical pathology, and hematopathology at New York Hospital/Cornell Medical Center, and was a research fellow at Princeton University. Dr. Chen received her Ph.D. from Oregon Health & Science University, and earned her medical degree from Hunan Medical University. She is board certified in Clinical & Anatomic Pathology, and Hematopathology.
Dr. Chen's research deals with the structure, function and regulation of anti-self antibodies. There are two types of anti-self antibodies: the antigen-induced autoantibodies which arise during a typical T-cell dependent immune response (to self-antigens), and the so-called natural autoantibodies which are expressed "ospontaneously" in the course of normal B cell development. The former are usually of high affinity and exist only in autoimmune individuals, whereas the latter often have low reactivity towards a wide spectrum of self-antigens and are present in all individuals, ordinarily without causing pathology. Using transgenic and knock-in mouse models that express Ig genes encoding various types of autoantibodies, we have shown that production of high affinity anti-self antibodies is prevented in normal mice by several mechanisms including killing or inactivating the B-cells that make such antibodies, or by secondary rearrangement of the Ig genes (receptor editing). In sharp contrast, B cells that express low affinity natural autoantibodies are not eliminated, but rather are preferentially expanded, indicating important physiologic function of these antibodies. We have recently discovered that expression of natural autoantibodies in autoimmune mice can ameliorate disease and improve survival. Our current study is focused on the mechanisms by which natural autoantibodies and B cells protect from autoimmune diseases.