HPTN (HIV Prevention Trials Network) Network Laboratory (NL) is responsible for collecting, testing and reporting results from biological samples; assisting in the development and quality assurance assessment of local laboratory capacity at the Clinical Trials Units (CTUs) participating in HPTN clinical trials (www.hptn.org); and identifying and implementing state-of-the-art assays and technologies to advance the scientific agenda of the Network.

Research in the Steven Frank Lab focuses on processes to improve blood use and to avoid blood transfusions for patients who do not want to receive blood or blood products. Processes include autologous hemodilution and cell salvage, and treating or averting anemia pre- and post-surgery. Other lab studies have focused on blood conservation, bloodless medicine surgery, the regulation of body temperature during surgery and methods of preventing hypothermia during surgery.

The Krummey Lab is a part of the Department of Pathology at the Johns Hopkins School of Medicine.

Our research prioritizes understanding the cellular mechanisms of alloimmunity, with a concentration on manipulating various cosignaling receptors and antigen recognition pathways to restrain the key lymphocytes principally involved in graft rejection. With the use of MHC tetramers, transgenic mouse models, and high-dimensional flow cytometry, we focus on mouse- and human-graft specific CD8+ T cells, CD4+ T cells, and B cells.

Transplantation is a life-saving procedure against a variety of diseases. Despite technical advances vastly improving early outcomes after transplant, long-term survival of transplanted organs has remained stagnant for the better part of three decades. A major cause of graft loss is immune-mediated rejection, which traditionally has be classified as acute or chronic based on its occurrence early or late after transplantation. Recently, this consensus has shifted to defining a graft rejection by its immunologic characteristics, either antibody-mediated or T cell-mediated (cellular rejection). This is because modern discoveries have identified the true major contributor to graft failures that occur many years after transplantation: not chronic rejection, but rather the cumulative impact of T cell-mediated acute rejection as a risk factor for later graft loss. Thus, original approaches to specifically prohibit and/or treat T cell-mediated acute rejection are of major significance for improving post-transplant outcomes.

HLA compatibility has also proven to be paramount for graft rejection. Originally, this was believed to be at the cellular level, then the single HLA protein level, and now at the epitope or molecular mismatch level. Specifically, HLA class II epitope-level mismatch has been identified as a risk factor for graft rejection, and multiple studies have identified specific epitopes within HLA class II peptides that are thought to be highly pathogenic. Few techniques directly measure antibody responses against specific regions of HLA proteins, but such measurements could provide both new information about the strength and character of alloimmunity and serve as an important new tool to study allogeneic B cells and antibody-secreting cells.