Deficiency of Interleukin2 Inhibitor Activity in Serum from Autoimmune-Prone Mice

Kazuo Kobayashi The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Tsuyoshi Kasama The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Toshtyuki Fukushima The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Ketta Kasahara The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Minoru Tabata The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Fusao Sekine The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Masao Negishi The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Hirotsugu Ide The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

Teruml Takahashi The First Department of Internal Medicine, School of Medicine, Showa University, 1–5–8 Hatanodal Shinagawa-ku, Tokyo, 142, Japan

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Abstract

To study the mechanisms that regulate the activity of Interleukin 2 (IL 2) and possibly limit its activity, we have examined normal mouse serum for their ability to Inhibit IL 2-mediated proliferation of a cloned IL 2-dependent cytotoxic T lymphocyte line (CTLL). Normal mouse serum contains a factor capable of inhibiting IL2 dependent proliferation of CTLL cells. This factor is absorbed with IL 2-dependent cells, but not with IL 2 molecules. Decreased activity of the inhibitor is observed in serum from autoimmune-prone mice such as NZB and NZBWF1 hybrid mice. The results suggest that the serum IL 2 inhibitor may play an important role In the in vivo regulatory mechanism of IL 2 activity and that lack of the Inhibitor may be associated with aberrant immune functions.

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Deficiency of Interleukin2 Inhibitor Activity in Serum from Autoimmune-Prone Mice

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Deficiency of Interleukin2 Inhibitor Activity in Serum from Autoimmune-Prone Mice

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