Mouse CD30 is a protein consisting of 498 amino acids and is a member of the TNF receptor family. It is characterized by repeated cysteine-rich motifs in the extracellular domain. Murine CD30, compared to the human protein, has a 90 amino acid gap in the extracellular region that seems to be duplicated in human CD30. CD30 is a type I trans-membrane glycoprotein, and it is expressed on some B cells and on mitogen-stimulated T cells. CD30 was originally identified as a cell surface antigen, Ki-1, on Hodgkin and Reed-Sternberg cells. CD30 binds to CD30L, a type II transmembrane protein, and the CD30-CD30L interaction induces NF-κB activation, which is mediated by TNFR-associated factor 2 (TRAF2). CD30L/CD30 signaling seems to be involved in Th1 and Th2 cell responses and plays a key role in Th17 differentiation in mice. TNFRs, such as CD30, OX40, and 4-1BB participate in the survival of activated T cells. Mice lacking both OX40 and CD30 signals have severe loss of CD4+ memory T cells in the spleen and lamina propria. Also, CD30-deficient mice show a decreased capacity to sustain follicular germinal center responses, and double KO mice (OX40 and CD30) lack memory antibody responses because of deficiency in CD4 T cell memory. Mast cells are the predominant CD30L-positive cells in chronic inflammatory skin diseases such as psoriasis and atopic dermatitis, and CD30 and CD30L expression is upregulated in lesional skin in these conditions. An agonistic anti-CD30 drug conjugate, Brentuximab vedotin, has been approved for the treatment of CD30-positive lymphomas.