Abstract
Tubercule bacilli disperse following aerosol infection from the lungs systemically and enter latency in the majority of subjects. Despite their hematogenic spread, the bacilli reactivate in most cases in the lungs. This chapter reviews knowledge about the host cellular reactions, cytokines, cell adhesion molecules, and receptors possibly involved in the mechanisms behind this predilection. Valuable data came from comparison of the levels of cellular and humoral mediators in the bronchoalveolar lavage and plural or other effusions with those in the blood. The analysis concerned both the initial infection and the subsequent reactivation leading to severe pathology. Granuloma formation, representing the key histopathology, can restrain the multiplying bacilli but can also develop into necrotic cavitary lesions. Immunoregulatory factors have been of interest for better understanding of the pathogenesis. The reviewed knowledge helps to illuminate how the minority of latently infected subjects develop active tuberculosis (TB) and may also be useful for improving vaccination and developing adjunct immunotherapies for TB.
Original language | English |
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Title of host publication | Mucosal Immunology (Fourth Edition) |
Editors | Jiri Mestecky |
Place of Publication | USA |
Publisher | Elsevier Inc. |
Pages | 1817 - 1830 |
Volume | 2 |
Edition | Fourth |
DOIs | |
Publication status | Published - 15 Mar 2015 |