title: TNF in host resistance to tuberculosis infection.
abstract: TNF is essential to control Mycobacterium tuberculosis infection and cannot be replaced by other proinflammatory cytokines. Overproduction of TNF may cause immunopathology, while defective TNF production results in uncontrolled infection. The critical role of TNF in the control of tuberculosis has been illustrated recently by primary and reactivation of latent infection in some patients under pharmacological anti-TNF therapy for rheumatoid arthritis or Crohn's disease. In this review, we discuss results of recent studies aimed at better understanding of molecular, cellular and kinetic aspects of TNF-mediated regulation of host-mycobacteria interactions. In particular, recent data using either mutant mice expressing solely membrane TNF or specific inhibitor sparing membrane TNF demonstrated that membrane TNF is sufficient to control acute M. tuberculosis infection. This is opening the way to selective TNF neutralization that might retain the desired anti-inflammatory effect but reduce the infectious risk.
authors.affiliation: Molecular Immunology and Embryology UMR6218, Orleans University and CNRS, Orleans, France. quesniaux@cnrs-orleans.fr
authors.forename: Valerie F J
authors.initials: VF
authors.lastname: Quesniaux
authors.forename: Muazzam
authors.initials: M
authors.lastname: Jacobs
authors.forename: Nasiema
authors.initials: N
authors.lastname: Allie
authors.forename: Sergei
authors.initials: S
authors.lastname: Grivennikov
authors.forename: Sergei A
authors.initials: SA
authors.lastname: Nedospasov
authors.forename: Irene
authors.initials: I
authors.lastname: Garcia
authors.forename: Maria L
authors.initials: ML
authors.lastname: Olleros
authors.forename: Yuriy
authors.initials: Y
authors.lastname: Shebzukhov
authors.forename: Dmitry
authors.initials: D
authors.lastname: Kuprash
authors.forename: Virginie
authors.initials: V
authors.lastname: Vasseur
authors.forename: Stephanie
authors.initials: S
authors.lastname: Rose
authors.forename: Nathalie
authors.initials: N
authors.lastname: Court
authors.forename: Rachel
authors.initials: R
authors.lastname: Vacher
authors.forename: Bernhard
authors.initials: B
authors.lastname: Ryffel
mesh_terms: D000818:Animals; D057134:Antibodies, Neutralizing / Q000009:adverse effects; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000276:immunology; D008213:Lymphocyte Activation; D008262:Macrophage Activation; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D018448:Models, Immunological; D009169:Mycobacterium tuberculosis / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014376:Tuberculosis / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000172:deficiency / Q000235:genetics / Q000276:immunology*
chemical_list: D057134:Antibodies, Neutralizing; D014409:Tumor Necrosis Factor-alpha