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Published October 1, 1984 | public
Journal Article

High-level secretion of interleukin 2 by a subset of proliferating thymic lymphoblasts

Abstract

We have characterized the thymocytes that can be induced to secrete interleukin 2 (IL 2) after polyclonal stimulation with Con A. For maximal activation, an important adjunct to the Con A is the phorbol ester TPA. In the presence of TPA, IL 2 production by thymocytes is relatively independent of adherent accessory cells; this allows us to compare the abilities of different thymic subpopulations to make IL 2. The most numerous class that includes IL 2 producers is made up of cells with a typical "medullary" population, the phenotype: moderately small, postmitotic cells that fail to bind peanut agglutinin. In addition, however, a population of large, proliferating lymphoblasts is competent in IL 2 production directly as isolated. Relative to the total "medullary" population, the lymphoblasts are enriched for the ability to make IL 2. They account for a significant proportion of the total IL 2 produced by thymocytes, and demonstrate that this aspect of immunocompetence is not restricted to cells that have finished their intrathymic proliferation. The IL 2-producing lymphoblasts do not bind peanut agglutinin or express thymus-leukemia antigen, but they do express high levels of Lyt-1. Although distinct from most medullary thymocytes, therefore, they are also distinct from the majority of cortical blast cells for which a direct precursor role has been established. They may be a subset of the rare proliferating blast cells in the medulla. Further heterogeneity in the thymic IL 2 producers is demonstrated by their expression of the Lyt-2 glycoprotein. The majority of IL 2 producers are Lyt-2^- as are the majority of peripheral T "helper" cells. However, a distinct minority of the thymic IL 2 producers express Lyt-2. Therefore, the ability of some peripheral Lyt-2^+ cells to secrete IL 2 may be determined at the time of their initial programming in the thymus.

Additional Information

© 1984 American Association of Immunologists. Received for publication April 3, 1984. Accepted for publication May 22, 1984. The costs of publication of this article were defrayed In part by the payment of page charges. This article must therefore be hereby marked advertisement In accordance with 18 U.S.C. Section 1734 solely to Indicate this fact. This work was supported by Grants Al 19752 and Al 16769 from the National Institutes of Health and by National Cancer Institute Grant CA 14195 to the Armand Hammer Cancer Center of the Salk Institute. Recipient of a Fellowship from the Alberta Heritage Foundation for Medical Research.

Additional details

Created:
August 19, 2023
Modified:
October 24, 2023