Research

Dr. Koralov is a cellular and molecular immunologist with experience in studying the molecular and cellular etiology of autoimmune and malignant diseases. His past projects focused on V(D)J recombination, lymphomagenesis and the role of RNAi in lymphocyte biology. Dr. Koralov’s research has previously helped characterize the molecular mechanisms of secondary IgH recombination and defined the role of RNAi in B cell survival and proliferation.

We are now taking advantage of a strong foundation in immunology and expertise in conditional gene targeting and molecular biology to pursue projects related to autoimmunity, cancer and basic B and T cell development.

The goal of the first project is to explore the role of Th17 driven inflammation in asthma and psoriatic arthritis. For this purpose we are taking advantage of biospecimens from patients as well as novel mouse models of disease. We are able to dissect the contribution of Th17 cells to chronic inflammation in the airways, skin and bone; determine the role of antigen receptor specificity and explore the role of microbiota and microbial metabolites in these inflammatory diseases.

We are also interested in furthering our understanding of malignant transformation of T lymphocytes and in particular have been focused on understanding the pathogenesis of an enigmatic hematologic malignancy, Cutaneous T Cell Lymphoma (CTCL). This cancer is characterized by accumulation of malignant cells in the skin, where they are exposed to bacterial and environmental antigens. We have been studying the contribution of antigen receptor signaling and bacterial antigens and super antigens in the malignant transformation of T cells using a unique mouse model of this disease as well as through analysis of patient biospecimens.

Another project in the lab focuses on the role of RNAi in B cell development, differentiation and function. The emphasis of this project is to both explore the role of individual miRNAs in maintaining lymphoid identity and to understand the contribution of RNAi to Ig locus accessibility during V(D)J recombination, somatic hypermutation and class switch recombination. Our aim is to gain better understanding of the regulation of these dangerous genetic events and to dissect the various ways in which non-coding RNAs contribute to normal B cell development and function, as well as to lymphomagenesis.

A relatively new area of research for our group leverages our expertise in studying tissue specific inflammation to understand the mechanisms of immune suppression and evasion in the context of lung cancer and melanoma. We aim to understand how tumor metabolism subverts immune responses and our goal is to take advantage of our insight to improve current immunotherapy modalities in a patient specific manner.