Authors
Andrew R Crow, Vinayakumar Siragam, Davor Brinc, Seng Song, John Freedman, and Alan H Lazarus
Summary
While strides have been made in the understanding of how intravenous immunoglobulin (IVIg) ameliorates autoimmune diseases by using mouse models of immune thrombocytopenia (ITP) and inflammatory arthritis, the precise cellular target of IVIg has remained elusive. To determine which cell populations interact with IVIg upstream of the inhibition of phagocytosis, we have developed a method for ‘priming’ specific leukocyte populations with IVIg to study their potential role in ameliorating ITP upon passive transfer, which we describe herein. Using this technique, we found that splenic CD11c+ dendritic cells reacted with IVIg, or several IVIg mimetic regimes, were primed to ameliorate ITP upon transfer to thrombocytopenic mice. We anticipate that this novel methodology could also be used to determine the mechanism of action of IVIg in other autoimmune diseases in addition to ITP.Further details
The protocol was published on Protocol Exchange in 2006. To see the entire protocol, click on the source link.Advertisement
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