Although the initial Th1 and Th2 subsets are relatively stable, recent studies have demonstrated some flexibility and plasticity, particularly in other CD4 T cell subsets. Cytokines and other soluble mediators in the lymph node and inflamed tissue can further affect the cytokine expression profile of effector CD4 T cells [3] , in some cases by changing the differentiation status of the effector CD4 T cells. Primed precursor CD4 T (Thpp) cells, that produce mainly IL-2 and chemokines when stimulated, remain uncommitted with respect to their effector cytokine pattern and can later differentiate into either Th1 or Th2 cells [4] [5] [6] . Suppressive Treg cells, expressing the forkhead transcription factor Foxp3, can lose the expression of Foxp3 and acquire the ability to produce pro-inflammatory cytokines during autoimmunity [7] . Th17 cells can acquire the ability to produce IFNc in Th1 polarizing conditions [8, 9] . Adoptively transferred IL-4-producing Th2 effector cells can produce IFNc during viral challenge infections [10] . Th9 cells develop from Th2 populations in the presence of TGFb [11, 12] and T follicular helper (Tfh) cells may represent a further differentiation step from several of the other subsets [13] .