Fabian Benencia, PhD
Associate Professor, Immunology
Academic Research Center 202C
Member Type: Investigator
My research explores the capability of antigen presenting cells to act as inducers or suppressors of immunity responses in different diseases such as cancer, atherosclerosis or infections. These cells are keystones of the immune response, being capable of triggering specific immunity. Thus, they have been used for vaccination purposes. In pathological conditions, they can be involved in inflammatory diseases, collaborating with tissue injury. On the other hand, they can collaborate with tumor growth by suppressing the specific anti-tumor immune response or inducing tumor vascularization. Investigating the factors governing the phenotype plasticity of these cells may unhide new targets for immune therapies.
In addition, I am also interested in the involvement of these cells in different inflammatory conditions:
Diabetes: In a collaborative work with Dr. Kelly McCall, also a DI investigator at OU, I am studying the phenotype of the immune populations at the level of draining lymph nodes and pancreas in models of infection-induced diabetes. To this end, we recover cells from the aforementioned organs resected from normal or TLR3-KO mice and we identify the different immune populations present, and their degree of activation by flow cytometry analysis.
Obesity: Through a collaborative research with Dr. Darlene Berryman, DI Director, I am investigating the characteristics of different immune cell populations, in particular macrophages, monocytes, DCs and T cells in different fat depots recovered from normal and growth hormone over-producing mice. Determining the nature of immune cells such as inflammatory macrophages, which are claimed to contribute to promote obesity, in different depot tissues can help generate targeting therapies to fight diseases associated with obesity such as diabetes or cancer.
Benencia, F., Harshman, S., Duran-Ortiz, S., Lubbers, E. R., List, E. O., Householder, L., … Berryman, D. E. (2015). Male bovine GH transgenic mice have decreased adiposity with an adipose depot-specific increase in immune cell populations. Endocrinology, 156(5), 1794–1803.
McCall, K. D., Thuma, J. R., Courreges, M. C., Benencia, F., James, C. B. L., Malgor, R., … Schwartz, F. L. (2015). Toll-like receptor 3 is critical for coxsackievirus B4-induced type 1 diabetes in female NOD mice. Endocrinology, 156(2), 453–461.
McCall, K. D., Schmerr, M. J., Thuma, J. R., James, C. B. L., Courreges, M. C., Benencia, F., … Schwartz, F. L. (2013). Phenylmethimazole suppresses dsRNA-induced cytotoxicity and inflammatory cytokines in murine pancreatic beta cells and blocks viral acceleration of type 1 diabetes in NOD mice. Molecules (Basel, Switzerland), 18(4), 3841–3858.
Osterbur, J., Sprague, L., Muccioli, M., Pate, M., Mansfield, K., McGinty, J., … Benencia, F. (2013). Adhesion to substrates induces dendritic cell endothelization and decreases immunological response. Immunobiology, 218(1), 64–75.