Edmond J. Feris1,§, Joaquin Zuñiga2,§, Liliana Encinales3, Joel N.H. Stern4,5, Julio Granados6, Marcelo Fernadez-Vina7 and Edmond J. Yunis3
1Department of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth, Lebanon,
NH 03765, USA
2Laboratory of Immunobiology and Genetics, Instituto Nacional de Enfermedades Respiratorias,
Mexico City, Mexico
3Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, MA 02115,
USA
4Department of Science Education, Hofstra North Shore-LIJ School of Medicine, Hempstead, NY 11549, USA
5Department of Neurology, North Shore- LIJ, Manhasset, NY 11030, USA
6Immunology and Rheumatology Department, Instituto Nacional de Ciencias Medicas y Nutricion México City, Mexico
7Department of Pathology, Stanford University School of Medicine, Stanford, CA 94304, USA
In previous report, we reported that anti tuberculin (IgG) antibodies and in vitro proliferation assays against tuberculin are better indicators of latent tuberculosis infection (LTBI) than the tuberculin skin test (TST). We concluded that these tests are markers of LTBI regardless of the level of exposure and TST results. We now report that, the blocking of proliferation responses was only produced in the cultures with tuberculin and not Candida suggesting a crosstalk between the two antigens influence cellular immunity and not humoral immunity. Most important is the fact that although cellular immunity plays a central role in the pathogenesis of active and latent tuberculosis, humoral immunity is dominant in LTBI. In this regard, recent evidence demonstrated that conserved genes of Mycobacterium tuberculosis coding the epitopes that induce T cell dependent are naturally selected; the immune response benefits the mycobacteria. Therefore, we emphasize the need to use humoral immune mechanisms in the diagnosis and control of mycobacterium infection.
§These authors contributed equally.