@Article{ecn.2007.0083,
AUTHOR = {Muazzam Jacobs, Arina Samarina, Sergei Grivennikov, Tania Botha, Nasiema Allie, Cecile Fremond, Dieudonnée Togbe, Virginie Vasseur, Stephanie Rose, Francois Erard, Analbery Monteiro, Valerie Quesniaux, Bernhard Ryffel},
TITLE = {Review: Reactivation of tuberculosis by tumor necrosis factor neutralization},
JOURNAL = {European Cytokine Network},
VOLUME = {18},
YEAR = {2007},
NUMBER = {1},
PAGES = {5--13},
URL = {http://www.techscience.com/ECN/v18n1/66016},
ISSN = {1952-4005},
ABSTRACT = {Tumor necrosis factor (TNF) is required in the control of infection with <i>Mycobacterium tuberculosis</i>
(Mtb), the causative agent of tuberculosis. TNF is essential and non-redundant for forming microbiocidal
granulomas, and cannot be replaced by other members of the TNF family. We established a model of latent Mtb
infection in mice, allowing investigation of the reactivation of latent Mtb as observed in patients receiving
TNF-neutralizing therapy used in rheumatoid arthritis and Crohn’s disease. Antibody neutralization of TNF is
able to reactivate clinically silent Mtb infection. Using mutant mice expressing solely membrane, but not soluble
TNF, we demonstrated that membrane TNF is sufficient to control acute Mtb infection. Therefore, we hypothesize
that TNF-neutralizing therapy, sparing membrane TNF, may have an advantage as compared to complete
neutralization. In conclusion, endogenous TNF is critical for the control of tuberculosis infection. Genetic absence
or pharmacological neutralization of TNF results in uncontrolled infection, while selective neutralization might
retain the desired anti-inflammatory effect but reduce the infectious risk.},
DOI = {10.1684/ecn.2007.0083}
}