Cyclosporin A, a fungal metabolite, is a novel antilymphocytic agent with significant immunosuppressive effects. It strongly inhibits the appearance of direct and indirect plaque-forming cells (PFC) in mice and dose-dependently suppresses hemagglutinin formation. Cyclosporin A delays skin graft rejection and graft-versus-host disease (GvH) in mice and rats, and prevents paralysis in rats with experimental allergic encephalomyelitis. It effectively prevents Freund's adjuvant arthritis and improves symptoms in established arthritis, though it is inactive in acute inflammation. Unlike other immunosuppressants, cyclosporin A has low myelotoxicity and acts on an early stage of mitogenic triggering in immunocompetent lymphoid cells. Cyclosporin A, a cyclic peptide with 11 amino acids and a molecular weight of 1202.6, was isolated from *Cylindrocarpon lucidum* and found in *Trichoderma polysporum*. It was tested for effects on humoral and cellular immunity, inflammatory conditions, and other pharmacological actions. Due to its poor water solubility, it was administered as a suspension in tragacanth. Control animals received the solvent. The study used various methods to assess cyclosporin A's effects, including hemolytic plaque-forming cells (PFC) assays, hemagglutination tests, and GvH disease models. Results showed that cyclosporin A significantly inhibited both direct and indirect PFC, with effects lasting up to 8 days after administration. It also suppressed GvH disease in mice and rats, and improved arthritis symptoms. Cyclophosphamide and azathioprine showed similar or more pronounced effects in some cases. Statistical significance was determined using Student's t-test. The study highlights cyclosporin A's unique immunosuppressive properties and its potential as a new therapeutic agent.Cyclosporin A, a fungal metabolite, is a novel antilymphocytic agent with significant immunosuppressive effects. It strongly inhibits the appearance of direct and indirect plaque-forming cells (PFC) in mice and dose-dependently suppresses hemagglutinin formation. Cyclosporin A delays skin graft rejection and graft-versus-host disease (GvH) in mice and rats, and prevents paralysis in rats with experimental allergic encephalomyelitis. It effectively prevents Freund's adjuvant arthritis and improves symptoms in established arthritis, though it is inactive in acute inflammation. Unlike other immunosuppressants, cyclosporin A has low myelotoxicity and acts on an early stage of mitogenic triggering in immunocompetent lymphoid cells. Cyclosporin A, a cyclic peptide with 11 amino acids and a molecular weight of 1202.6, was isolated from *Cylindrocarpon lucidum* and found in *Trichoderma polysporum*. It was tested for effects on humoral and cellular immunity, inflammatory conditions, and other pharmacological actions. Due to its poor water solubility, it was administered as a suspension in tragacanth. Control animals received the solvent. The study used various methods to assess cyclosporin A's effects, including hemolytic plaque-forming cells (PFC) assays, hemagglutination tests, and GvH disease models. Results showed that cyclosporin A significantly inhibited both direct and indirect PFC, with effects lasting up to 8 days after administration. It also suppressed GvH disease in mice and rats, and improved arthritis symptoms. Cyclophosphamide and azathioprine showed similar or more pronounced effects in some cases. Statistical significance was determined using Student's t-test. The study highlights cyclosporin A's unique immunosuppressive properties and its potential as a new therapeutic agent.