Peripheral CD4+ T cells can be divided into several functional subsets, including type 1 helper (Th1), type 2 helper (Th2), type 17 helper (Th17), and regulatory T (Treg) cells. Th1, Th2, and Th17 cells are collectively called effector Th cells. Each subset of effector Th cells secretes a unique combination of cytokines and plays a distinct role in regulating adaptive immunity. However, effector Th cells can also contribute to the pathogenesis of allergic inflammation and various organ-specific autoimmune diseases, if their function is not regulated properly. Thus, the functional balance among various subsets of Th cells can critically influence the outcomes of these diseases.
Despite the striking differences in function, all subsets of CD4+T cells are differentiated from T cell precursors originating from bone marrow common lymphoid precursors. Further maturation and differentiation of common lymphoid precursors is controlled by a complicated genetic cascade involving several subset-specific or non-specific transcriptional factors and cytokines.
My laboratory researches the transcription factors that are important for the development and function of various subsets of CD4+T cells. The factors of interest include c-maf, GATA-3, ROG, and Ets-1. We has generated various “knock-out” mouse strains, each of which is rendered deficient in one of the transcription factors. These knock-out strains provide us with a great opportunity to study the in vivo regulatory roles of the transcription factors. Studies on these mice may uncover novel targets for manipulation of the differentiation of Th cells and, subsequently, the function of Th immune responses. Such manipulation may be beneficial in allergic and autoimmune diseases.