Dr. Kraig's laboratory focuses on aging and its effects on immune regulation. They were first to report that humoral responses to a protein antigen decline with age, while memory immunity to the same antigen is maintained. Moreover, they showed that recall of memory B and T cells from one's youth could result in late onset autoimmunity. Current efforts are focused in three areas. First, they have shown that baboons maintain efficacious humoral (B cell and T cell) responses into old age. By comparing immune parameters across non-human primate species and assessing how baboons are unique should provide insights into optimizing vaccines for use in older individuals. Second, using a murine model of myasthenia gravis, they study the effects of aging on immunity, autoimmunity, and tolerance. Lastly, they have pursued the fascinating finding that an immunosuppressive drug, rapamycin, could increase longevity in mice, even when the treatment was initiated relatively late in life. Since older individuals have diminished immune competence, it seemed counter-intuitive that further assaults on their immune systems. Yet, surprisingly, no detrimental effects were seen and in fact, the rapamycin treated animals showed improvement in their humoral responses to bacteria. Since the effects of rapamycin were different in old mice from those seen in adult animals, a small pilot study was initiated in elderly humans (>85 years of age) in collaboration with Dr. Dean Kellogg. Thus far, rapamycin appears to be safe, even in very old individuals, and could be considered as an adjunct therapy for improving vaccine efficacy with age.
Dr. Kraig is primarily involved in teaching graduate courses. She directs the Graduate Colloquium Course for PhD students and the Presentation Skills Course for MS students. These courses are designed to give students an opportunity to hone their skills in reading the scientific literature and preparing clear research seminars. In addition, she contributes to other graduate courses, with lectures on immunology and molecular biology. Dr. Kraig received the UTHSCSA Presidential Award for Teaching Excellence in 1996, the Dean's Award for Exceptional Graduate Teaching in 2000, and she was elected to the UT Academy of Health Science Educators in 2007.
In addition, Dr. Kraig serves as the Deputy Chair of Faculty Development in the department and Chairs SUCCEED, a committee dedicated to the successful career development of our students, postdoctoral fellows, and faculty.
Stacy S, Williams EL, Standifer NE, Pasquali A, Krolick KA, Infante AJ, Kraig E
Maintenance of immune tolerance to a neo-self acetylcholine receptor antigen with aging: implications for late-onset autoimmunity.
J Immunol. 2010 Jun 1;184(11):6067-75.
Stacy S, Pasquali A, Sexton VL, Cantwell AM, Kraig E, Dube PH.
An age-old paradigm challenged: old baboons generate vigorous humoral immune responses to LcrV, a plague antigen. J Immunol. 2008 Jul 1;181(1):109-15.
Standifer NE, Stacy S, Kraig E, Infante AJ.
Discrete T cell populations with specificity for a neo-self-antigen bear distinct imprints of tolerance. J Immunol. 2007 Mar 15;178(6):3544-50.
Infante AJ, Baillargeon J, Kraig E, Lott L, Jackson C, Hämmerling GJ, Raju R, David C.
Evidence of a diverse T cell receptor repertoire for acetylcholine receptor, the autoantigen of myasthenia gravis. J Autoimmun. 2003 Sep;21(2):167-74.
Standifer NE, Kraig E, Infante AJ.
A hierarchy of T cell receptor motifs determines responsiveness to the immunodominant epitope in experimental autoimmune myasthenia gravis. J Neuroimmunol. 2003 Dec;145(1-2):68-76.
Stacy S, Gelb BE, Koop BA, Windle JJ, Wall KA, Krolick KA, Infante AJ, Kraig E
Split tolerance in a novel transgenic model of autoimmune myasthenia gravis.
J Immunol. 2002 Dec 1;169(11):6570-9.
Stacy S, Krolick KA, Infante AJ, Kraig E.
Immunological memory and late onset autoimmunity.
Mech Ageing Dev. 2002 Apr 30;123(8):975-85.
Majumder S, Caccamo A, Medina DX, Benavides AD, Javors MA, Kraig E, Strong R, Richardson A, Oddo S.
Lifelong rapamycin administration ameliorates age-dependent cognitive deficits by reducing IL-1β and enhancing NMDA signaling. Aging Cell. 2012 Apr;11(2):326-35.