RECIPROCAL REGULATION OF CD30 EXPRESSION ON CD4(-CELLS BY IL-4 AND IFN-GAMMA() T)

Prior studies have implicated CD30 as a marker for Th2 cells, but the mechanism that underlies this correlation was unknown. We show here th at CD30 was expressed on activated CD4(+) T cells in the presence of I L-4. In the absence of endogenously produced IL-4, however, even Th2 l ineage cells lost CD30 expression. Thus, CD30 is not an intrinsic mark er of Th2 cells, but is inducible by IL-4. CD30 was also found to be d own-regulated by IFN-gamma. Committed Th1 effector cells do not expres s CD30, although differentiating Th1 lineage cells temporarily express CD30. The transient expression of CD30 on differentiating Th1 lineage cells was mainly the result of endogenously produced IL-4 induced by IL-12. Culture of IL-12-primed cells under conditions that reverse the phenotype (Ag plus IL-4) resulted in two cell populations based upon their ability to express CD30. One population responded to IL-4 upon r estimulation and became a CD30-positive, Th0-like cell population, whi le the other remained CD30 negative and synthesized only IFN-gamma. Th us, CD30 expressed on CD4(+) T cells reflected the ability of CD4(+) T cells to respond to IL-4.