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Freund, Gregory G. Deszo, Eric Louis 2015-09-25T21:08:07Z 2015-09-25T21:08:07Z 10000-01-01 2003 2003 The data in this thesis indicate one, that the removal of the tyrosine phosphatase CD45 enhances activation of protein kinase C delta (PKCdelta), and two, PKCdelta activity in conjunction with STAT6 regulate the expression of the co-stimulatory marker B7.2 (CD86) and three, the expression of CD86 and the production of cytokines in phorbol-12-myristate-13-acetate (PMA)-stimulated promyelocytes is regulated by calcium calmodulin kinase kinase alpha. These data together indicate that promyelocyte differentiation is a process that is dependent on the activity of PKCdelta. Furthermore, this process is subject to regulation by interlukin-4 induced STAT6 activation and CaMKKalpha. In conclusion we have identified possible targets for future therapies in the treatment of diabetes induced altered immunity. Made available in DSpace on 2015-09-25T21:08:07Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 3086046.pdf: 7119636 bytes, checksum: 2ecc7c3ddd2d64c7c1577974e556349d (MD5) Previous issue date: 2003 Embargo set by: Seth Robbins for item 84832 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs U of I Only 145 p. Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2003. http://hdl.handle.net/2142/83551 (MiAaPQ)AAI3086046 eng Health Sciences, Pathology Molecular Mechanisms of Promyelocyte Maturation: Implications for Immune Dysfunction in Type II Diabetes text Animal Sciences Animal Sciences University of Illinois at Urbana-Champaign Dissertation Ph.D.