Next Article in Journal
Verapamil Inhibits TRESK (K2P18.1) Current in Trigeminal Ganglion Neurons Independently of the Blockade of Ca2+ Influx
Next Article in Special Issue
Harmful Effects and Potential Benefits of Anti-Tumor Necrosis Factor (TNF)-α on the Liver
Previous Article in Journal
Time Dependent Pathway Activation of Signalling Cascades in Rat Organs after Short-Term Hyperoxia
Previous Article in Special Issue
Bimodal Function of Anti-TNF Treatment: Shall We Be Concerned about Anti-TNF Treatment in Patients with Rheumatoid Arthritis and Heart Failure?
Article Menu
Issue 7 (July) cover image

Export Article

Open AccessArticle

Transmembrane TNF and Partially TNFR1 Regulate TNFR2 Expression and Control Inflammation in Mycobacterial-Induced Pleurisy

Department of Pathology and Immunology, Centre Medical Universitaire (CMU), Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland
Centre National de la Recherche Scientifique, UMR7355, and Experimental and Molecular Immunology and Neurogenetics, University of Orléans, 45100 Orléans, France
Author to whom correspondence should be addressed.
Present address: Laboratory of Integrative Immunology, National Institute of Respiratory Diseases “Ismael Cosio Villegas”, Mexico City 14080, Mexico.
Int. J. Mol. Sci. 2018, 19(7), 1959;
Received: 13 April 2018 / Revised: 15 June 2018 / Accepted: 30 June 2018 / Published: 4 July 2018
(This article belongs to the Special Issue Tumor Necrosis Factor (TNF))
PDF [1719 KB, uploaded 4 July 2018]


Pleural tuberculosis is one of the most frequent forms of extra-pulmonary tuberculosis observed in patients infected with Mycobacterium tuberculosis. Tumor Necrosis Factor (TNF) is a crucial cytokine needed to control tuberculosis infection that remains a leading cause of morbidity and mortality worldwide. TNF blockade compromises host immunity and may increase the risk of reactivation of latent infection resulting in overt pulmonary, pleural and extra-pulmonary tuberculosis. While TNF signaling is mainly considered pro-inflammatory, its requirement for the anti-inflammation process involved in the resolution of infection and tissue repair is less explored. Our study analyzes the role of TNF and TNF receptors in the control of the inflammatory process associated with Bacillus Calmette-Guérin (BCG)-induced pleurisy. This study shows that the absence of TNF causes exacerbated inflammation in the pleural cavity of BCG-infected mice which is controlled by the transmembrane TNF (tmTNF) expression. The lack of TNF is associated with an impaired cellular expression and shedding of TNFR2 in the pleural cavity. The presence of tmTNF restores the normal expression of TNFR2 on myeloid cells during BCG-induced pleurisy. We also show that absence of TNFR1 affects the expression of TNFR2 on pleural cells and inflammation in the pleural cavity of BCG-infected mice. In conclusion, tmTNF but not soluble TNF prevents pleural cavity inflammation leading to attenuation and the resolution of the inflammatory process caused by mycobacterial pleurisy in association with the expression of TNFR2 on myeloid cells. View Full-Text
Keywords: TNF; TNF receptors; BCG-induced pleurisy; inflammation TNF; TNF receptors; BCG-induced pleurisy; inflammation

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Uysal, H.; Chavez-Galan, L.; Vesin, D.; Blaser, G.; Benkhoucha, M.; Ryffel, B.; Quesniaux, V.F.J.; Garcia, I. Transmembrane TNF and Partially TNFR1 Regulate TNFR2 Expression and Control Inflammation in Mycobacterial-Induced Pleurisy. Int. J. Mol. Sci. 2018, 19, 1959.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top