Human autoimmune diseases are specific antigen-driven T-cell diseases: identification of the antigens
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Human autoimmune diseases are specific antigen-driven T-cell diseases: identification of the antigens Chris D. Platsoucas Æ Emilia L. Oleszak
Published online: 23 May 2007 Ó Humana Press Inc. 2007
Abstract We are investigating the hypothesis that most human autoimmune diseases are specific antigen-driven T-cell diseases. T-cell clones responding to specific antigenic epitopes are responsible for the initiation and/or the propagation of these diseases. Similarly, specific antigen-driven T-cell responses are responsible for the rejection of organ allografts and the immune response to tumors. Activated T cells provide the ‘‘engine’’ for the chronic inflammation that is associated with autoimmune diseases, organ graft rejection and tumor immunity. The best way to identify whether specific antigen-driven T cell responses are involved in the initiation and/or propagation of these disorders is to investigate whether T cells that infiltrate relevant tissues from these diseases contain monoclonal or oligoclonal, that is to say clonally expanded, populations of T cells. Identification of the T-cell antigen receptor (TCR) transcripts employed by the clonally expanded T cells in
Presented at the First Robert A Good Society Symposium, St. Petersburg, FL 2006. This paper is devoted to the memory of Dr. Robert A. Good, the founder of modern human immunology. In addition to his landmark scientific discoveries, Dr. Good trained over 350 postdoctoral fellows, graduate students and other scientists. Most of them are now serving as Department Chairs and Professors in the US and abroad, investigating with their students immunological problems. Dr. Good’s impact in training the next generations of immunologists has been unique and profound. To continue Dr. Good’s legacy several of his students have formed in 2005 The Robert A. Good Immunology Society (Chris D. Platsoucas, Ph.D., Founding President) with the objective of ‘‘(a) promoting and fostering the field of immunology and related areas;’’ ‘‘(b) encouraging the development of new ideas and the exchange of information between: (i) immunology and related disciplines; (ii) basic and clinical investigators in immunology, molecular genetics and bone marrow transplantation, and (c) encouraging the involvement of students, young scientists and physicians in the field of immunology and the above disciplines and fostering their development into accomplished investigators.’’ (see Bylaws of the Robert A. Good Immunology Society). C. D. Platsoucas (&) Department of Microbiology and Immunology, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA e-mail: [email protected] E. L. Oleszak Department of Anatomy and Cell Biology, Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, USA
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Immunol Res (2007) 38:359–372
these patients permits the identification of the specific antigens that elicit these T-cell responses. These antigens may be responsible for the pathogenesis of these disea
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