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Dr Thomas Lehner, Professor of Basic and Applied Immunology; London University. Qualifications: MB, BS London, MD London, FDS RCS, FRC Path, F Med Sci Prizes and Honours Besredka Prize of the Pasteur Institute, Lyon, France. Honorary Doctorate, Karolinska Institute, Stockholm, Sweden Honorary Life President of the International Society for Behcet’s Disease Appointed Commander of the British Empire (CBE) Honorary Fellow of the Royal Society of Medicine Selected International appointments Member of NIH (NIAID), Bethesda US Review Committee Research Grants 1999-2007. Member of Scientific Committee of the International Mucosal Immunology 1997-2006 Member of the Scientific Committee of the Institute of Virology of the University of Maryland (1998-2002). Research Career A total of 265 peer-reviewed papers published in scientific journals. Over the past 20 years research carried out in animals and humans, preventing HIV and SIV infections. Focussed on mucosal immunisation, generation of CC-chemokines, CCR5 coreceptors stress agents and alloimunisation. Major research grants from the MRC, NIH, European Union, Gates Foundation.
HIV infection affects 37 million people and about 1.7 million are infected annually. Only the RV144 vaccine phase III clinical trial elicited significant protection against HIV-1 acquisition, but the efficacy and immune memory were inadequate. To boost these two critical functions of the vaccine we studied T stem cell memory (TSCM) and innate immunity. TSCM cells were identified by phenotypic markers of CD4+ Tcells and they were further characterised into 4 subsets. These consisted of IL-2/IL-15 receptors and APOBEC3G anti-viral restriction factors, which were upregulated, whereas CCR5 co-receptors and ?4?7 mucosal homing integrins were decreased. A parallel increase in CD4+ T cells was recorded of the IL-15 receptors, APOBEC3G and CC chemokines, with a decrease in CCR5 expression. We suggest a novel mechanism of dual memory stem cells; the established sequential memory pathway, TSCM ?Central ?Effector memory CD4+ T cells and the innate pathway consisting of the 4 subsets of TSCM. Both pathways are likely to be activated by endogenous HSP70, the hallmark of cellular stress. The memory stem cells and innate immunity pathways should be optimised to boost the efficacy and immune memory of protection against HIV-1. TSCM are likely to be activated by inducible HSP70, as PES (phenylethynesulphonamide), a small molecular inhibitor induced a dose-dependent inhibition of TSCM. The link between memory stem cells and innate immunity suggests a novel mechanism of inhibiting HIV-1 acquisition, by decreasing CCR5 and ?4?7, increasing IL-15/IL-2 receptors and HIV-1 restriction factors