UNIVERSITY OF CALIFORNIA, SAN FRANCISCO 
BERKELEY • DAVIS • IRVINE • LOS ANCELES • RIVERSIDE • SAN DIECO • SAN FRANCISCO 
SANTA BARBARA • SANTA CRUZ 
SCHOOL OF MEDICINE 
DEPARTMENT OF MEDICINE 
Please address reply 10 the undersigned at 
Immunology and Arthritis Section (151 T) 
Veterans Administration Hospital 
4150 Clement Street 
San Francisco, California 94121 
April 5, 1979 
Wallace P. Rowe, M.D. 
Chief, Laboratory of Viral Diseases 
National Institute of Allergy and 
Infectious Diseases 
National Institutes of Health 
Bethesda MD 20205 
Dear Wally: 
In reply to your letter of March 22, I believe that there 
are very strong constraints against the development of 
autoimmune disease in most instances. By contrast, auto- 
antibody formation without disease occurs with surprising 
frequency, particularly in aged individuals, those suffering 
from chronic infections, or under treatment with drugs such 
as procainamide. In the last situation, 50% will develop 
anti-nuclear factor, but only 1% actually get drug-induced 
lupus. The symptoms disappear rapidly when the drug is 
discontinued, although the autoantibodies can persist 
for months.^ 
The secretory IgA system in the gastrointestinal tract is a 
strong barrier against immunity to bacterial or ingested 
products. In IgA deficient individuals, immunization to 
such materials can occur. ^ 
I am enclosing a reprint of a theoretical paper that distinguishes 
between auto-recognition (which is physiologic and necessary 
for proper immunologic communication), autoimmunity, and autoimmune 
disease. Please let me know if I can be of further help. 
NT: th 
1. Lee SL, Chase PM: Drug-induced systemic lupus 
erythematosus: a critical review. Sem Arthritis Rheum 
5:83-103, 1975. 
2. Anmann A J , Hong R: Selective IgA deficiency. Medicine 
50:223-236, 1971. 
Sincerely yours 
Norman Talal, M.D. 
Professor of Medicine 
[ 247 ] 
