Reversal by interferon‐γ of inhibition of delay ed‐type hypersensitivity induction by anti‐CD4 or antiinterleukin 2 receptor (CD25) monoclonal antibodies. Evidence for the physiological role of the CD4+ TH1+ subset in mice

In mice, induction of delayed-type hypersensitivity (DTH) and of antibody formation to sheep red blood cells (SRBC) was inhibited by the anti-CD4 monoclonal antibody (mAb) GK1.5. However, anti-interleukin 2 mAb AMT-13 inhibited DTH response but not antibody formation. The inhibitory action of the mAb on DTH, but not an antibody formation, was reversed by concomitant injection of recombinant mouse interferon-gamma. These data provide the first in vivo evidence for the postulated physiological role of the CD4+ TH1 lymphocyte subset and indicate that the action of anti-interleukin 2 receptor mAb is restricted to this T helper subset.