1
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Interleukin 2 in cell-mediated immune responses.

      , , , ,
      Journal of supramolecular structure
      Wiley

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The lymphokine Interleukin 2(IL2) restores T cell responses in a number of in vitro systems where immunogenicity has been compromised. UV irradiation of the stimulating allogeneic cells in a mixed leukocyte culture eliminates the production of cytotoxic T lymphocytes and greatly reduces the DNA synthesis response. IL2 restores both parameters. UV-irradiated stimulators are also unable to induce the normal production of IL2 which is observed in a mixed leukocyte culture. The cytotoxic activity of allogeneically stimulated thymocytes is almost completely lost within 24 hours after removal of IL2 at 5 days, indicating that the lymphokine is continuously required to maintain CTL. Thymocytes in 4-day cultures do not adsorb IL2 unless they are simultaneously activated with a mitogen. Finally, IL2 does not adequately restore a secondary response to the purified protein derivative of tuberculin (PPD) in adherent-cell-depleted cultures, indicating that macrophages, in addition to being required for IL2 production, have other functions. These probably include the presentation of soluble antigens to responding cells.

          Related collections

          Author and article information

          Journal
          J. Supramol. Struct.
          Journal of supramolecular structure
          Wiley
          0091-7419
          0091-7419
          1980
          : 13
          : 2
          Article
          10.1002/jss.400130214
          6972471
          ac7e7ebc-2542-46fb-b579-d709289ec3ae
          History

          Comments

          Comment on this article