Abstract | Keywords | Export | Availability | Bookmark

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Tuberculosis, a systemic mycobacteriosis produced by M. tuberculosis and M. Bovis, affects the lung (pulmonary forms) as well as the other organs of the body (extra pulmonary forms). Infection induces the formation of an inflammatory granuloma and the involvement of tributary lymph nodes: a stage no apparent clinical lesions referred to as primary infection. Recovery is due to cellular immunity and relies on the presence of T lymphocyte activated macrophages. A progression of the infectious process entails the production of radiologically detectable lesions (primary tuberculosis including actives and inactive forms). Re-infection of recovered patients, or proliferation of mycobacteria from an existing focus, produce more extensive lesions, which ca progress and possibly heal (active and inactive post-primary tuberculosis). Extra pulmonary tuberculosis may develop in any organ or tissue (hematogenous dissemination from existing lesions).
Diagnosis of tuberculosis relies on clinical, radiological and microbiological examination. Immunoassays are susceptible of helping diagnosis and prognosis.
The complex immune response elicited by a mycobacterial infection results from an interaction of different bacterial components with the host immune system. Cellular immunity plays a key role in the development of anti-tuberculosis immunity, whereas humeral immunity has a secondary role. The delayed hypersensitivity reaction which is triggered by tuberculin injection, is just an example of the cell-mediated response.
The role played by humeral immunity in the host defense against mycobacteria is unknown : an enhancement of phagocytes of opsonized micro organisms has been suggested. However, the level of circulating antibodies might reflect the evolution of tuberculosis processes.
We have described the preparation of antigen A60 from the cytoplasm of Mycobacterium bovis BCG; the antigen was purified by exclusions gel chromatography and lectin affinity chromatography. Its identity was established by two-dimensional immunoelectrophoresis. Antigen 60 is located intracellular during the exponential phase, but is partially released extra cellular in the course of the declining phase.

Antigens, bacterial --- Tuberculosis --- Mycobacterium tuberculosis