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Immunological relatedness of the protective mechanisms against tuberculosis and cancer
Author(s) -
Carlo Cocito,
Hubert Maes
Publication year - 1998
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1998.00248.x
Subject(s) - lymphokine , adoptive cell transfer , immune system , immunology , cytolysis , tumor necrosis factor alpha , tuberculosis , cancer research , antigen , cancer , t cell , medicine , biology , cytotoxicity , in vitro , pathology , biochemistry
Background Bacille Calmette–Guérin (BCG), an attenuated strain of tuberculous bacillus, is the source of vaccines providing unclear and variable protection against tuberculosis (TB) and cancer. Thermostable macromolecular antigens (TMAs) are major mycobacterial complexes immunodominant in disease. A60 (TMA complex of BCG) protects mice against TB development, via T lymphocyte (TL)‐mediated macrophage (MΦ) activation, halting intracellular mycobacterial replication. In most A60‐primed mice, cytolytic TLs and MΦ infiltrate cancer tissue, resulting in 80–100% rejection. Adoptive TL transfer is indispensable for MΦ‐dependent tumour cell inactivation via oxygen and nitrogen radicals. Neoplasm development induces immune anergy with depletion of A60‐specific TL and activated MΦ. A60 protects mice against TB and cancer by inducing the synthesis of three lymphokines: interleukin 2 (IL‐2), interferon gamma (IFN‐γ) and tumour necrosis factor alpha (TNF‐α). Tumour cells prevent A60‐dependent synthesis of these lymphokines in vivo and in vitro . Conclusion These data provide some clues to immune surveillance and tumour escape mechanisms, as well as to the antituberculous and antineoplastic BCG action.