Dr. Keith Krolick profile photo

Contact

Department

Microbiology, Immunology & Molecular Genetics

Krolick, Keith A., Ph.D.

Adjunct Professor

Personal Statement:

Dr. Krolick’s formal training was in Microbiology and Immunology, following which, as a tenured member of the UT Health San Antonio graduate faculty, he performed continuously funded research in areas of immunology (particular emphasis on autoimmune disease) for over 30 years while training numerous doctoral students.

Dr. Krolick subsequently shifted his emphasis from laboratory research to the educational and administrative missions of the Graduate School. He taught in all six schools of the UT Health San Antonio, in both basic science and pre-clinical science courses for PhD and MS students, and for medical, dental, and nursing students. He also served as the director of several graduate level and pre-clinical courses.

Dr. Krolick was the inaugural Program Director for the Integrated Biomedical Sciences (IBMS) Graduate Program of the Graduate School of Biomedical Sciences, as well as the head of the Microbiology & Immunology component of the Integrated Biomedical Sciences Graduate Program. Dr. Krolick also sought and received approval from the THECB for the Master of Science in Immunology & Infection program and served as its inaugural Program Director.

Dr. Krolick was selected as a member of the UT Health San Antonio Academy of Master Teachers, the Long School of Medicine’s Academy of Educational Scholars, and as a University of Texas System Distinguished Teaching Professor. He was also selected as a member of the UT System Kenneth I. Shine Academy of Health Science Education. Dr. Krolick was awarded the UTHSCSA Presidential Award for Sustained Excellence in Teaching and the UT System Regents’ Outstanding Teacher’s Award.

Education

B.S., University of Illinois, Champaign/Urbana
Ph.D., Immunology at the University of California, Los Angeles
Postdoctoral Training, UT Southwestern Medical Center, Dallas

Research

The distinction between ‘self’ and ‘non-self’ must be made in order to guarantee beneficial rather than detrimental immunity. Thus, autoimmunity (immunity against one’s self), the focal point of a variety of health problems, has been the central theme of Dr. Krolick’s interests. For thirty years, his laboratory used numerous strategies for studying one particular autoimmune disease, myasthenia gravis (MG). Even after Dr. Krolick closed his lab, he continued to pursue his interests in immunology via contributions to the educational missions of the university.

What he learned in those 30 years… In MG, one of 40 or so muscle diseases classified as muscular dystrophy, antibodies produced by one’s own immune system against muscle acetylcholine receptors (AChR) leads to muscle damage and impaired nerve-muscle communication. The symptoms of MG include weakness and rapid-onset fatigue.

Contrary to what was once believed, his lab learned that the relationship between AChR antibody production and disease induction is not simple. That is, from individual-to-individual, the severity of disease symptoms and the aggressiveness of disease progression are not strictly correlated with the amount of AChR antibody that an individual produces. Two major observations were the driving force behind much of Dr. Krolick’s work:

Observation 1: The exact fine specificity of an AChR antibody determines the level of resulting interference with neuromuscular transmission. Unless an antibody binds to the receptor at exactly the right spot, no effect on contractile function will be observed. Different individuals produce mixtures of AChR antibodies that demonstrate different T lymphocyte-determined proportions of the disease-causing subset, and therefore differences in disease symptom severity.

Observation 2: Soluble and cell-membrane factors, originating from muscle, have the ability to either amplify or inhibit immune responses. It was very exciting to consider that the various pathological outcomes in MG individuals may be based on the fact that the target tissue (i.e., muscle) is not just sitting there getting ‘beat up’ and that disease severity is not determined simply by the intensity of the antibody response itself.

Clearly, muscle has the capacity to produce factors that promote resistance to, and repair of, the damage done by the immune system and plays an active, not passive, role in determining disease outcome. Curiously, most of these muscle-derived factors are cytokines, chemokines, and adhesion molecules that are also produced by cells of the immune system, making communication with the immune system highly efficient.

Moreover, the stimuli that trigger the production of these muscle-derived factors often come from the stimulated immune system itself. Therefore, a circular communication path back to the immune system exists that determines the composite set and intensities of cells of the immune system that participate in subsequent rounds of immune responsiveness and muscle pathology and the severity of symptoms demonstrated by an individual.

Awards & Accomplishments

• UT System Regents’ Outstanding Teacher’s Award
• UT Health San Antonio Presidential Award for Sustained Excellence in Teaching
• Member, Long School of Medicine’s Academy of Educational Scholars
• Member, UT System Kenneth I. Shine Academy of Health Science Education
• UT System Distinguished Teaching Professor
• UT Health San Antonio Academy of Master Teachers
• University of Texas System Distinguished Teaching Professor
• UT Health San Antonio Leadership Education & Development (LEAD) Institute

Affiliations

  • American Association of Immunologists (1981)
  • International Society of Neuroimmunology (1989)

Publications

  • Stacy S. Williams EL. Standifer NE. Pasquali A. Krolick KA. Infante AJ. Kraig E. (2010) Maintenance of immune tolerance to a neo-self acetylcholine receptor antigen with aging: implications for late-onset autoimmunity. J. Immunol., 184:6067-75.
  • Shandley S. Martinez S. Krolick K. (2009) IL-4 Receptor as a Bridge Between the Immune System and Muscle in Experimental Myasthenia Gravis I. Up-regulation of Muscle IL-15 by IL-4. Clinical Immunol., 132:246-56.
  • Krolick K.A. (2006) Muscle-Derived Nitric Oxide Synthase Expression, Differences Associated With Muscle Fiber-type, and Disease Susceptibility in a Rat Model of Myasthenia Gravis. Clin. Immunol., 121:286-293.
  • Garcia, Y.R. and Krolick, K.A. (2004) Short-circuiting autoimmune disease by target-tissue-derived nitric oxide. Clin Immunol. 113:74-80.
  • Garcia, Y.R., Pothitakis, J.C., and Krolick, K.A. (2003) Myocyte production of nitric oxide in response to AChR-reactive antibodies in two inbred rat strains may influence disease outcome in experimental myasthenia gravis. Clin. Immunol., 106:116-126.
  • Reyna-Reyes, S., Stegall, T. and Krolick, K.A. (2002) Muscle responds to an antibody reactive with the acetylcholine receptor by up-regulating monocyte chemoattractant protein 1: a chemokine with the potential to influence the severity and course of experimental myasthenia gravis. J. Immunol., 169:1579-1586.
  • Stegall, T. and Krolick, K.A. (2001) Myocytes respond in vivo to an antibody reactive with the acetylcholine receptor by upregulating interleukin-15: an interferon-gamma activator with the potential to influence the severity and course of experimental myasthenia gravis. J. Neuroimmunol., 119:377-386.