Author Affiliations: Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut (Dr Milstone). Dr Waksman retired, formerly affiliated with Yale University School of Medicine.
Readers of a recent article published in the Archives about the usefulness of an interferon- γ release assay in diagnosing erythema induratum1 might like to put that work in historical and technical perspective. Many years ago, a medical student (L.M.M.), wondering why lymphocytes infiltrated virus-infected tissues, teamed up with an immunologist (B.H.W.) working in the emerging field of lymphokines. They hypothesized that sensitized lymphocytes challenged by a specific antigen might release an inhibitor of viral replication. Since tuberculin reactivity was a standard (and nonviral) manifestation of delayed-type hypersensitivity, they took lymphocytes from mice immunized with PPD (purified protein derivative, used in tuberculosis skin testing), challenged them in vitro with PPD, and found that those lymphocytes secreted an inhibitor of vesicular stomatitis virus growth.2 That secreted inhibitor eventually became known as interferon- γ, and the basics of that original test have been recapitulated in several interferon- γ release assays for tuberculosis.3
Milstone LM, Waksman BH. Interferon- γ Release Assay. Arch Dermatol. 2012;148(1):133–134. doi:10.1001/archdermatol.2011.2077