Gregory A. Viglianti, Ph.D.
Associate Professor of Microbiology
BA, Lafayette College
PhD, University of Minnesota
Postdoctoral Training, Harvard University
Mucosal immune responses of the lower female reproductive tract to sexually transmitted pathogenic microorganisms leads to an inflammatory response that enhances the heterosexual transmission of HIV-1. Inflammation is initiated largely by signaling through members of the Toll-like family of innate immune receptors that are activated by pathogen-encoded ligands. This inflammatory response enhances HIV-1 transmission by inducing the recruitment of target immune cells such as Langerhans/dendritic cells (LC/DC), macrophages (MØ)‚ and T lymphocytes to the mucosa and by direct activation of these cells. Recent findings have demonstrated that activation of certain nuclear receptors (NR), including peroxisome proliferator activated receptor (PPAR), liver X receptor (LXR), and glucocorticoid receptor (GR)) potently inhibits TLR-induced inflammatory gene expression in MØ, LC/DC, and epithelial cells. Studies in the Viglianti laboratory are directed toward evaluating the ability of ligand-activated NR to inhibit the mucosal transmission of HIV-1 and to determine the molecular mechanism(s) of how ligand-activated NR inhibit TLR-induced transcription of both HIV-1 and inflammatory cytokine genes.
Autoimmune diseases such as systemic lupus erythematosus (SLE) are characterized by the overproduction of antibodies, many of which recognize ribonucleoprotein and/or chromatin related autoantigens. A common feature of these autoantigens is that they include DNA or RNA. The Viglianti laboratory, in collaboration with Dr. Ann Marshak-Rothstein, is defining the protein and nucleic acid composition of these immunostimulatory autoantigens and determining whether different forms of apoptosis are capable of selectively releasing these autoantigens from cells, thereby making them accessible to autoreactive B cells.