Sergei B. Koralov

Currently my laboratory is focused on the following questions: 1. How do Th17 cells promote chronic inflammation? We are using several animal model of chronic inflammation that we developed in the lab (COPD and Psoriatic Arthritis) to understand the genesis of tissue specific inflammation. In particular, we are examining the role of antigen stimulation and environmental triggers (namely microbiota and microbial metabolites) in potentiating Th17 mediated chronic inflammation. 2. What is the role of antigen stimulation and microbiota in malignant T cell transformation? We are using a newly established animal model of CTCL and our state of the art gnotobiotic facility to complement our studies of patient biospecimens to address the role of T cell Ag receptor and microbial antigens in the malignant transformation of T lymphocytes. Our focus is on Cutaneous T Cell Lymphoma (CTCL), an enigmatic malignancy of T lymphocytes, characterized by the striking dermal tropism of the malignant cells. 3. What is the role of tumor intrinsic metabolic changes in the suppression of the cancer-specific immune responses? We are taking advantage of our unique access to patient biospecimens and our cutting-edge mouse genetics to dissect how tumors subvert immune surveillance by changing their metabolic profile. Our focus is currently on lung cancer. 4. What is the role of non-coding RNAs in lymphocyte development and function? The emphasis of this project is to both explore the role of individual miRNAs in maintaining lymphoid identity, survival and proliferation; and to understand the contribution of RNAi to Ig locus accessibility during V(D)J recombination, somatic hypermutation and class switch recombination.