doi: 10.1016/S1071-5576(02)00259-9. while others indicating that RUPP rat closely mimics many features of PE, including elevations in blood pressure and B cells and preproendothelin in the placenta, blood vessels, and the kidney of RUPP rats (8, 11, 16, 22, 25). In particular, LaMarca et al. (11) reported that rituximab, used to deplete B cells, reduced blood pressure, B cells, and autoantibodies to the angiotensin II type I Indirubin-3-monoxime receptor (AT1-AA), placental preproendothelin, IL-6, and TNF-. Importantly, while B cells may not be increased in women with PE compared with normal pregnant women, there is mind-boggling evidence that they are activated and secrete soluble factors and antibodies that contribute to the pathogenesis of PE (9, 27). It is important to address the differences in experimental methods that might explain the divergent results. B cells are the secretors of all antibodies. They are generally divided into two classes: B1 and B2. B1 cells produce natural antibodies that primarily consist of IgM and IgA and some IgG, which are very different from adaptive antibodies produced from B2 cells. Rat B1 cells express CD19+CD5+CD23?CD43+ (1, 7, 9, 21, 27, 30). B2 cells are the standard B cells that Indirubin-3-monoxime produce all types of antibodies, as well as specialized antibodies such as IgG types 1C4 as a part of the adaptive immune response. Rat B2 cells express CD19+CD5?CD23+CD43? (13). Laule et al. (12) used IgM+ Rabbit Polyclonal to GSK3alpha and CD11b to distinguish between circulating, splenic, and placental B1 and B2 cells. Although CD11b can be used to distinguish between types of B1 cells found in the plural and peritoneal cavity, splenic B1 cells do not express this marker (7). Moreover, CD11 is not a favored marker distinguishing B2 cells at any stage in the life cycle. IgM was also used as a marker for B cells by Laule et al. but is present on many B cells, especially plasma B cells. Therefore, IgM is not a distinguishing marker among B1 and B2 cells. Laule et al. used IgM and CD11 to differentiate B1 from B2 cells; however, these two cell types cannot be distinguished by these markers alone, as outlined in their study. In addition, Laule et al. indicated the purpose of their study was to determine the effect of depleting B1 independently from other B cells by using anti-CD20. Unfortunately, there is no methodology to completely deplete B1- from other B-cell populations in animals. Moreover, this could not be achieved with an anti-CD20 in rats or humans. However, this is an important area of investigation and would be an exciting find which could be very useful for treating autoimmune diseases and would be a major advancement for malignancy immunopharmacology. B cells are the source of AT1-AA, which has been consistently shown by several laboratories from different institutions to Indirubin-3-monoxime be elevated in preeclamptic women and also found to be elevated in the RUPP rat model of PE (2, Indirubin-3-monoxime 5, 8, 9, 11, 16, Indirubin-3-monoxime 24, 26, 28, 29). Multiple studies from several laboratories have shown that infusing or injecting AT1-AA causes hypertension and many characteristics of PE (2C4, 8, 9, 11, 26, 28, 29). Moreover, administration of a specific peptide inhibitor of AT1-AA reduces the hypertension in the RUPP model (3, 4, 26, 28, 29). Thus, the question is not the importance of B cells secreting AT1-AA in preeclampsia, as has already been well established, but which type of B cell produces AT1-AA. Jensen and colleagues (9, 27) found that placental B1 cells can produce AT1-AA when stimulated by PE serum. Importantly, in the study of Laule et al. (12), anti-CD20 treatment did not reduce the expression of B1 cells in either the spleen or the placenta in treated.
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