Dr. Michael Eller obtained his Ph.D. in Immunology from the Karolinska Institutet, in Stockholm, Sweden focusing research on cellular immune functions through the course of natural HIV-1 natural infection in Ugandans. Dr. Eller served as the laboratory Co-Director for the Makerere University Walter Reed Project (MUWRP) in Kampala, Uganda from 2003 through 2009 where he was responsible for the specimen processing lab and immunological assay development in support of MHRP vaccine studies and natural history cohorts. Since moving back to the U.S., he continues to serve as Laboratory Director for the MUWRP lab, is the section head for the MHRP Flow Cytometry Laboratory (MFCL), and conducts basic research into the immunopathogenesis of HIV.
MHRP Flow Cytometry Laboratory (MFCL)
MFCL provides support to all researchers at MHRP, performing research-based cellular assays to assess immunogenicity for clinical trails and immune characterization in natural HIV-1 infection cohort studies. Multiparametric phenotyping of immune responses is rapidly becoming a central component for assessing protective immunity. Given that the mission of MHRP is the development and deployment of an efficacious prophylactic vaccine against HIV-1, the program must be able to assess and down-select candidate vaccines using the latest technology and currently accepted analysis schemes. The MFCL boasts capacity to conduct up to 16-color flow cytometry, live infectious sorting, and maintains a BD FACSCalibur™, two 4-laser LSR IIs, a 4-laser FACSAria™ SORP, and a Guava PCA.
Our laboratory focuses on the role of effector lymphocytes, both innate and adaptive, in HIV-infection and their contribution to viral control. Natural killer (NK) cells are considered vital to early protection from diseases and support development of adaptive immune responses. NK cells display a repertoire of activating and inhibitory molecules. KIR receptors have been a recent focus, where genetic association studies have implicated NK cells as contributors to control of HIV-1. We have shown NK cells exhibit skewed phenotype, including KIR expressing subsets, and altered function in chronic HIV-1 infection. NK cells support immune response through a variety of mechanisms: natural cytotoxicity, antibody dependent cellular cytotoxicity, cytokine/chemokine production and immune modulation through direct cell-to-cell interactions, however, less is known regarding NK cells in acute HIV infection. We aim to understand how NK cells may contribute to the initial control of HIV, during the earliest phase of infection, and characterize subsequent impact on disease progression.
One signature of HIV infection is immune activation, commonly characterized by aberrant T cell phenotypes. A number of mechanisms including soluble factors, microbial translocation, persistent antigen, and immune dysregulation are related to the increased frequency of activated T cells. The intricate network of associations between these factors, as well as markers of disease progression, suggest that systemic innate immune activation and chronic antigen stimulation both play important roles in driving pathological T cell phenotypes. We are particularly interested in studying the mechanisms behind the immunopathogenisis of HIV in acute HIV-1 infection, chronic infection, and after the initiation of antiretroviral therapy.