Defense Date


Document Type


Degree Name

Master of Science


Microbiology & Immunology

First Advisor

John Tew


The cause(s) of arthritis and many other connective tissue diseases are largely unknown. An infectious agent, either bacterial or viral, has not been unequivocally isolated. Theories on the pathogenesis of arthritis abound. Many of these theories implicate the immune system as the problem.

The early information on animal arthridites implicates retained bacterial cell wall antigens as the basis of the arthritis seen. How-ever, numerous types of antigens, both complex polymers and simple proteins, have been shown to persist in immune animals. The antigens persist in the lymph nodes and spleens playing a role in mediating antibody feedback mechanisms. Antigens also persist in collagenous tissues of the knees and feet of these animals. The role of retained antigen at these sites is unknown.

It is possible to induce arthritis in immune animals by administering antigen in the joint. Drawing from the information presented, I chose to explore the role of retained antigen on collagenous tissue in the pathogenesis of rheumatic diseases. This project is the continuation of work begun by J. G. Tew, T. E. Mandel, G. A. Miller, and A. W. Burgess. Through their research, the groundwork of antigen retention on the flexor and extensor tendons of immune mice was reported.


Scanned, with permission from the author, from the original print version, which resides in University Archives.


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VCU Theses and Dissertations

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Microbiology Commons