CSB Faculty

Sue C. Stacy, Ph.D.
Assistant Professor/Research

University of Texas Health Science Center at San Antonio, 2000

(210) 567-3848
STACYS@UTHSCSA.EDU

Dr. Stacy is a lecturer and lab instructor in the Gross Anatomy course for first year dental students. This course focuses on head and neck anatomy, embryology, and neurology. In addition, her laboratory research addresses the effects of age on B and T cell immunity, autoimmunity and immune tolerance.

In our laboratory studies, we are particularly interested in understanding the cellular and molecular aspects of the immune decline with age and how these alterations may be overcome in order to enhance the quality of life for the elderly. In one project we are studying the effects of recall immune memory. Although immune responses to new antigens often decrease with age, our lab and others have shown that immune responses to "recall" antigens (antigens first encountered in youth) are not severely diminished by aging. These long-lived responses might impact reactivity to newly encountered vaccine antigens in the elderly, either through by-stander help or through recalled suppression. Drs. Ellen Kraig, Peter Dube, and Sue Stacy are collaborating with the Southwest Primate Center to test this concept in a non-human primate model. A chimeric antigen is being employed to examine the ability of the tetanus "recall" response in old animals to modify B cell responses to a "new" antigen, LcrV (a protective antigen from the plague bacterium, Yersinia pestis). The concept is also being tested in a mouse model to allow further analysis of the cellular mechanisms of the recall response.

In addition to the recall projects, we are addressing mechanisms that maintain immune tolerance in healthy individuals and that, when disrupted, may result in tolerance loss and contribute to autoimmunity. Importantly, age-associated immune dysfunction may alter tolerance mechanisms. This is suggested by reports of higher levels of serum autoantibodies in the elderly and by the late-age (>40 years of age) onset of certain autoimmune diseases, including myasthenia gravis (MG). In patients with MG auto-antibodies are directed against the muscle acetylcholine receptor (AChR) resulting in symptoms of debilitating muscle fatigue. To facilitate the study of the effects of age on tolerance and autoimmunity, a novel transgenic mouse model of autoimmune MG was developed by Drs. Ellen Kraig, Tony Infante, and Sue Stacy. Using this model, studies are currently underway to address the mechanisms of tolerance to the muscle AChR. Cellular and molecular techniques being used include analysis of cell division patterns of adoptively transferred fluorescently labeled T cells directed against AChR epitopes (as illustrated).

Research Techniques:
Labeling and tracking antigen-specific T cells
Monitoring T cell subsets by FACS
Analysis of antibody titer and heterogeneity by ELISA and isoelectric focusing
Recombinant protein production and purification

PUBLICATIONS:
Stacy, S., K.A. Wall, K.A. Krolick, A.J. Infante, and E. Kraig. 2003. Recall Immune Memory: A New Tool for Generating Late Onset Autoimmune Myasthenia Gravis. Mech Ageing Dev, 124:931.

Stacy, S., B. Gelb, B. Koop, J. Windle, K. Krolick, A.J. Infante, and E. Kraig. 2002. Split Tolerance in a Novel Transgenic Model of Autoimmune Myasthenia Gravis. J Immunol, 169: 6570.

Stacy, S., K.A. Krolick, A.J. Infante, and E. Kraig. 2002. Immunological memory and late onset autoimmunity. Mech Ageing Dev. 123:975.

Tanaka, N., L.L. Espey, S. Stacy, and H. Okamura. 1992. Epostane and indomethacin actions on ovarian kallikrein and plasminogen activator activities during ovulation in the gonadotropin-primed immature rat. Biol Reprod 46: 665.

Espey, L.L., N. Tanaka, S. Stacy, and H. Okamura. 1992. Inhibition of ovulation in the gonadotropin-primed immature rat by exogenous prostaglandin E2. Prostaglandins 43 (1): 67.