Citations |
Cherukuri, A., Cheng, P. C., & Pierce, S. K. (2001). The role of the CD19/CD21 complex in B cell processing and presentation of complement-tagged antigens.The Journal of Immunology, 167(1), 163-172. Krop, I., De Fougerolles, A. R., Hardy, R. R., Allison, M., Schlissel, M. S., & Fearon, D. T. (1996). Self-renewal of B-1 lymphocytes is dependent on CD19.European journal of immunology, 26(1), 238-242. Engel, P., Zhou, L. J., Ord, D. C., Sato, S., Koller, B., & Tedder, T. F. (1995). Abnormal B lymphocyte delevopment, activation, and differentiation in mice that lack or overexpress the CD19 signal transduction molecule. Immunity, 3(1), 39-50. Sato, S., Jansen, P. J., & Tedder, T. F. (1997). CD19 and CD22 expression reciprocally regulates tyrosine phosphorylation of Vav protein during B lymphocyte signaling. Proceedings of the National Academy of Sciences,94(24), 13158-13162. |
Description |
The 1D3 monoclonal antibody specifically reacts with mouse CD19, a 95 kDa transmembrane glycoprotein, a member of the Ig superfamily and a B cell-lineage differentiation antigen expressed by all the B lymphocyte development stages, except for the terminally differentiated plasma cells. CD19 associates with CD21, CD81 and MHC class II to form a multi-molecular complex that initiates the mature B lymphocyte activation by interaction with the B-cell receptors. CD 19 enhances the B cell proliferation, development and activation, and the maturation of memory B cells. In CD19-deficient mice, the generation and maturation of B lymphocytes in the bone marrow and periphery are affected. |