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J. Exp. Med.,
Volume 189, Number 2, January 18, 1999 413-422
By
From the * Basel Institute for Immunology, CH-4005 Basel, Switzerland; the Apoptosis of cells must be regulated both positively and negatively in response to a variety of
stimuli in the body. Various environmental stresses are known to initiate apoptosis via differential signal transduction cascades. However, induction of signals that may inhibit apoptosis is
poorly understood, although a number of intracellular molecules that mediate inhibition of apoptosis have been identified. Here we present a novel murine macrophage-specific 54-kD secreted protein which inhibits apoptosis (termed AIM, for apoptosis inhibitor expressed by
macrophages). AIM belongs to the macrophage scavenger receptor cysteine-rich domain superfamily (SRCR-SF), members of which share a highly homologous conserved cysteine-rich
domain. In AIM-deficient mice, the thymocyte numbers were diminished to half those in
wild-type mice, and CD4/CD8 double-positive (DP) thymocytes were strikingly more susceptible to apoptosis induced by both dexamethasone and irradiation in vivo. Recombinant AIM protein significantly inhibited cell death of DP thymocytes in response to a variety of
stimuli in vitro. These results indicate that in the thymus, AIM functions in trans to induce resistance to apoptosis within DP cells, and thus supports the viability of DP thymocytes before
thymic selection.
Third Department
of Internal Medicine, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan; and the § Second Department of Pathology, Niigata University School of Medicine,
Niigata 951-8510, Japan
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