Abstract

CD4(+) T helper (Th) lymphocytes represent a heterogeneous population of cells. In addition to type 1 (Th1) and type 2 (Th2) cells, another subset of CD4(+) effector Th cells has been discovered and named as Th17, because of its unique ability to produce interleukin (IL)-17. Studies in mice initially suggested that Th17 cells are the pathogenic cells in autoimmune disorders, whereas Th1 cells may behave rather as protective. Subsequent studies in humans demonstrated the plasticity of Th17 cells and their possibility to shift to Th1. The plasticity of Th17 to Th1 cells has recently been confirmed in mice, where it was found that Th17 cells seem to be pathogenic only when they shift to Th1 cells. Studies in humans also showed that Th17 cells are different than in mice because all of them express CD161 and exclusively originate from CD161(+) precursors present in umbilical cord blood and newborn thymus. While murine Th17 cells develop in response to IL-6, IL-1, and transforming growth factor (TGF)-beta, human Th17 cells originate from these CD161(+) precursors in response to IL-1beta and IL-23, the need for TGF-beta being controversial. Thus, we believe that studies in humans have better depicted human Th17 cells than studies in mice.