CD30 is a member of the tumor necrosis factor receptor superfamily whose normal physiologic expression is restricted primarily to relatively small subpopulations of activated T- and B-cells. In abnormal physiologic states, CD30 has been found on inflammatory cells in patients with a variety of chronic inflammatory diseases such as atopic dermatitis and asthma. In addition, malignant Reed-Sternberg and anaplastic large cell lymphoma cells express particularly high levels of CD30. Cells expressing CD30 have been shown to be activated and produce cytokines during inflammatory responses. SGN-35 is an antibody-drug conjugate that binds to human CD30, ablates CD30+ tumor cells in vitro, and strongly inhibits growth of HL and ALCL tumors in vivo. In the present study, the effects of SGN-35 on antigen specific secondary immune responses were evaluated. Compared to untreated cells, SGN-35 induced a dose-dependent inhibition of T cell proliferation, with maximum inhibition of 70% following antigen stimulation in vitro. In the hu-SCID mouse tetanus toxoid model, antigen-specific immunoglobulin responses in SGN-35 treated mice were much lower compared to untreated controls (p=0.0019). Taken together, these data demonstrate specific targeting of subsets of activated lymphocytes and suggest that SGN-35 may be employed clinically to decrease antigen specific cells and immunoglobulin that damage tissue in autoimmune and inflammatory diseases.