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Role of IL-3 in the Antiphospholipid SyndromeResearch Unit of Autoimmune Diseases, Department of Medicine 'B', Sheba Medical Center, Tel-Hashomer, Tel-Aviv University, Research Institute, Golda Medical Center (Hasharon Hospital), Petach-Tikva, Affiliated to Bar-Ilan University, Israel
Research Unit of Autoimmune Diseases, Department of Medicine 'B', Sheba Medical Center, Tel-Hashomer, Tel-Aviv University, Research Institute, Golda Medical Center (Hasharon Hospital), Petach-Tikva, Affiliated to Bar-Ilan University, Israel Antiphospholipid syndrome (APLS) is characterized by recurrent thromboembolic phenomena, thrombocytopenia and fetal loss. We describe various methods of induction of experimental APLS. These models were employed to study a variety of therapeutic agents including low dose aspirin, low molecular weight heparin, IVIG and thromboxane receptor antagonist. Because interleukin-3 (IL-3) is a multilineage cytokine affecting also megakaryocytes, is regarded as a 'good' cytokine in various stages of pregnancy and as low levels of IL-3 were recorded in APLS, it was logical to employ IL-3 as a therapy for APLS. Indeed, this treatment completely abrogated all the manifestations of experimental APLS. Furthermore, it was found that low dose aspirin most probably affect positively APLS via inducing an increased production of IL-3 by monocytes.
Key Words: Cytokines Interleukin-3 Autoimmunity Antiphospholipid syndrome
Lupus, Vol. 3, No. 4,
259-261 (1994) This article has been cited by other articles:
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