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Role of sarcolectin (SCL) and interferons in coordinated T cell clonal expansion

A Kaba1, L A Ilunga, C Chany

  • 1Université René Descartes-Paris V, Laboratoire des Interferons et de la Sarcolectine, Paris, France. akaba@infobiogen.fr

Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research
|June 7, 2000
PubMed

T cell multiplication is attributed to the growth factor interleukin-2 (IL-2), which is, however, only activated when a specific cell membrane-bound receptor can be expressed. We found in all human sera tested a lectin that we described and called sarcolectin (SCL). SCL is a molecularly cloned 55-kDa protein that stimulates DNA synthesis in all immunocompetent cells and inhibits the interferon (IFN)-dependent antiviral state. SCL is excreted in conditioned medium of T cell cultures grown under serum-free conditions, where it can be demonstrated regularly by Western blots. In such cultures, in addition to SCL and IL-2, IFN-gamma and IFN-alpha also can be found, likely as a feedback response to DNA stimulation. Considered together, the data suggest that coordinated clonal expansion of T cells is governed by SCL-IL-2, both which induce T cell proliferation and simultaneously activate IL-2 receptors. T cell replication is downregulated by the effect of feedback IFN-gamma and IFN-alpha. To initiate a new growth cycle, SCL is thought to block the residual IFN-dependent antiproliferative state.

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