Randall G. Worth, Ph.D.
Office: HEB 239
Deans Award for Teaching Excellence - UT College of Medicine and Life Sciences, 2008
Dr. Worth is interested in the role of platelets in inflammation and infection. Two main projects are currently active to elucidate the immune function of platelets. First, Dr. Worth's laboratory has developed a conditional platelet-depletion mouse strain that is useful in studying the in vivo function of platelets during infections or other diseases. At a basic science level, Dr. Worth is interested in identifying pathways involved in pathogen destruction by platelets and leukocytes within host phagolysosomes. His laboratory has identified certain membrane domains that participate in phagocytosis and may also be important in mediating phagosome-lysosome fusion. Dr. Worth also heads a translational project directed at understanding the role of platelets in autoimmune diseases (Systemic Lupus Erythematosus). This project is revealing exciting new ways that platelets respond to IgG-complexes and the important interface between thrombosis and inflammation.
Current Grant Funding:
25. Ali, R.A., Wuescher, L.M., Worth R.G. 2015. Platelets: essential components of the immune system. Current Trends in Immunology. 16:65-78.
24. Wuescher, L.M., Takashima, A., Worth, R.G. 2015. A novel conditional platelet depletion mouse model reveals the importance of platelets in protection against S. aureus bacteremia. J. Thomb. Haemost. 13:303-313.
23. Dodd, D.A., Worth, R.G., Rosen, M.K. , Grinstein, S. , van Oers, N. S.C. , Hansen, E.J. 2014. The Haemophilus ducreyi LspA1 protein inhibits phagocytosis by using a new mechanism involving activation of C-terminal Src kinase. mBio 5(3):e01178-14. doi:10.1128/mBio.01178-14.
22. Cortes, C., Saggu, G., Emch, H.N., Ramirez, G., Worth, R.G., Ferreira, V.P. 2013. Identification of a novel mode of complement activation on stimulated platelets mediated by properdin. J. Immunol. 190:6457-67.
21. Dearth, C.L, Goh, Q., Marino, J.S., Cicinelli, P.A., Torres-Palsa, M.J., Pierre, P., Worth, R.G., Pizza,F.X. 2013. Skeletal muscle cells express ICAM-1 after muscle overload and ICAM-1 contributes to the ensuing hypertrophic response. PLoS One. 8(3):e58486.
20. Woodman, M.E., Worth, R.G., Wooten, R.M. 2012. Serum opsonization promotes the efficient uptake and killing of Burkholderia pseudomallei via induction of NADPH-oxidase by human neutrophils. PLOS One. 7(12):e52276.
19. Berlacher, M.D., Vieth, J.A., Heflin, B.C., Gay, S.R., Antczak, A.J., Singh, N., Montel, A.H., Kahaleh, M.B., Worth, R.G. 2013. FcγRIIa ligation induces platelet hypersensitivity to thrombotic stimuli. Am. J. Pathol. 182:244-54.
18. Vieth, J.A., Kim, M-k., Glaser,D., Stiles, K., Schreiber, A.D., Worth,R.G. 2013. FcγRIIa requires lipid rafts but not co-localization into rafts, for effector function. Inflamm. Res. 62:37-43.
17. Riaz, A.H., Tasma, B.E., Woodman, M.E., Wooten, R.M., Worth, R.G. 2012. Human platelets efficiently kill IgG-opsonized E. coli. FEMS Immunol. Med. Microbiol. 65:78-83.
16. Antczak, A.J., Vieth, J.A., Singh, N., Worth, R.G. 2011. Internalization of IgG-coated targets results in activation and secretion of soluble CD40 ligand and RANTES by human platelets. Clin. Vaccine Immunol. 18:210-216.
15. Vieth JA, Kim MK, Pan XQ, Schreiber AD, Worth R.G. 2010. Differential requirement of lipid rafts for FcγRIIA mediated effector activities. Cell. Immunol. 265:111-119.
14. Daniels, A.B., Worth, R.G., Dickstein, R.J., Dickstein, J.S., Kim-Han, T.H., Kim, M.K., Schreiber, A.D. 2010
Analysis of FcγRIIA cytoplasmic tail requirements in signaling for serotonin secretion:
evidence for an ITAM-dependent, P13K-dependent pathway. Scand J Immunol. 2010 71(4):232-239.
8. Kim, M-K, Hwang, P.-H., Huang, Z.-Y., Jones, B.A., Sato, N., Hunter, S. Kim-Han, T.-H, Worth, R.G., Indik, Z.K., Schreiber, A.D. 2003. Signal sequence Fcγ receptor transmembrane domains: Role in cell surface expression, gamma chain interaction and phagocytosis. Blood. 101:4479-4484.
7. *Worth, R.G., Kim, M-K., Kindzelskii, A.L., Petty, H.R., Schreiber, A.D. 2003. Signal sequence
within FcγRIIA controls calcium wave propagation patterns: apparent role in phagolysosome
fusion. Proc. Natl. Acad. Sci. USA, 100:4533-4538. * Reviewed in Research Roundup, “Calcium waves in membrane fusion,” J. Cell Biol. 161:221.
5. Worth R.G., Mayo-Bond L, Kim MK, van de Winkel JG, Todd RF 3rd, Petty HR, Schreiber AD. 2001. The cytoplasmic domain of FcgammaRIIA (CD32) participates in phagolysosome formation. Blood. 98(12):3429-34.
4. Worth, R.G., Esper, R.M., Warra, N.S., Rosenspire, A.J., Todd, III, R.F., Petty, H.R. 2001.
Mercury inhibition of neutrophil activity: evidence of aberrant cellular signaling
and incoherent cellular metabolism. Scan. J. Immunol. 53:49-55.
2. Petty, H.R., Worth, R.G., Kindzelskii, A.L. 2000. Imaging sustained dissipative patterns in the metabolism of individual living cells. Phys. Rev. Let. 84:2754-2757.
1. Worth, R.G., Mayo-Bond, L., van de Winkle, J.G.J., Todd III, R.F., Petty, H.R. 1996. CR3 (αmβ2; CD11b/CD18) restores IgG-dependent phagocytosis in transfectants expressing a phagocytosis defective FcγRIIA (CD32) tail minus mutant. J. Immunol. 157:5660-5665.