<i>Toxoplasma gondii</i> infection can regulate the expression of tumour necorsis factor‐α receptors on human cell <i>in vitro</i>

Derouich-Guergour, Dorra; Aldebert, Delphine; Vigan-Womas, Inès; Jouvin‐Marche, Evelyne; Marche, Patrice N; Aubert, Dominique; Ambroise-Thomas, P; Pelloux, Hervé

doi:10.1046/j.1365-3024.2002.00462.x

Cited by 24 publications

(21 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This study showed a maximal expression of TNF-R2 after infection at 4 h in both iDC and monocytes, which correlates well with the results from Belloni et al (18), who demonstrated a TNF-R2 up-regulation in Toxoplasma-infected THP-1 cells, also 3-4 h after infection with Toxoplasma. This is in contrast to another report that showed no increased expression of TNF-R2 after infection with Toxoplasma (29). Both of these studies used THP-1 cells in contrast to the iDC used in this study.…”

Section: Discussioncontrasting

confidence: 99%

Inhibition of the Growth ofToxoplasma gondiiin Immature Human Dendritic Cells Is Dependent on the Expression of TNF-α Receptor 2

Giese

Däubener

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

An effective immunity to Toxoplasma gondii in humans is dependent on the cellular immune response. Toxoplasma can infect and replicate in almost all nucleated cells, and the most important cytokine regulating the growth in humans is IFN-γ; however, the role of TNF-α has to date been largely described to be synergistic. We show that, compared with mature human dendritic cells (mDC), immature human DC (iDC) demonstrate a reduced parasite proliferation when infected with Toxoplasma. This toxoplasmostasis was only present in iDC after 11 days of culture and was not present in DC that had been matured ex vivo using a cytokine mixture (mDC). Spontaneous toxoplasmostatic activity has previously only been described in fresh human monocytes, and the mechanism involved is as yet unclear. We show that, in comparison with an absence of expression in mDC, TNF-R2 is expressed in both iDC and monocytes infected with Toxoplasma, and furthermore, that blocking the TNF-R2 with Abs abrogates the toxoplasmostasis in the iDC. These findings demonstrate a functional role for TNF-R2 in the newly described spontaneous toxoplasmostasis of iDC.

show abstract

Section: Discussioncontrasting

confidence: 99%

Inhibition of the Growth ofToxoplasma gondiiin Immature Human Dendritic Cells Is Dependent on the Expression of TNF-α Receptor 2

Giese

Däubener

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…A recent study reported a capability of T. gondii to regulate expression of TNFRs in vitro (Derouich-Guergour et al, 2002), as shown by an enhanced release of soluble TNFR1 from infected cells. The resistance of T.-gondii-infected fibroblasts to apoptosis induced by TNFα raises the possibility of a downregulation of TNFR1 or TNFR2 during infection.…”

Section: Discussionmentioning

confidence: 97%

Activation of NF-κB byToxoplasma gondiicorrelates with increased expression of antiapoptotic genes and localization of phosphorylated IκB to the parasitophorous vacuole membrane

Molestina

Payne

Coppens

et al. 2003

Journal of Cell Science

160

174

View full text Add to dashboard Cite

“…TRAPS presents clinically with self-limited inflammatory episodes (27). Therefore, in TRAPS patients, a proinflammatory event triggered by an environmental factor (such as infection [28,29], cancer [30,31], and drug toxicity [32]) that can up-regulate TNFRI expression will have an overall proinflammatory and antiapoptotic effect, because in the case of the T50K variant, which is capable of sustaining inappropriate NF-B activation, this will result in persistent production of proinflammatory mediators including TNF itself. A similar proinflammatory outcome has been shown in a mouse model of TRAPS (33).…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor receptor I from patients with tumor necrosis factor receptor–associated periodic syndrome interacts with wild‐type tumor necrosis factor receptor I and induces ligand‐independent NF‐κB activation

Yousaf¹,

Gould²,

Aganna³

et al. 2005

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. To investigate the molecular consequences of expressing mutated forms of tumor necrosis factor receptor I (TNFRI) as found in patients with TNFR-associated periodic syndrome (TRAPS).Methods. We cloned and expressed full-length wild-type (WT) and T50K and P46L variants of TNFRI using a new tightly regulated doxycycline-dependent expression system. This system enabled the study of molecular interactions between these receptors at both physiologic and pathophysiologic levels of expression.Results. We used chemical crosslinking on the cell surface to show that WT and mutant forms of TNFRI, derived from TRAPS patients, interact in the absence of TNF ligand. Doxycycline-controlled up-regulation of one TNFRI allele, either WT or mutant, caused downregulation of the other allele, indicating dynamic control of cell surface assembly. We also demonstrated that increased expression of mutant TNFRI (T50K) was associated with a parallel increase in NF-B p65 (RelA) subunit activation, which did not occur with increased expression of WT TNFRI.Conclusion. The T50K TRAPS-related variant is capable of sustaining inappropriate NF-B activation, resulting in persistent autoinflammation in target organs such as skin, synovial membrane, and the central nervous system. We conclude that some of the inflammatory processes seen in TRAPS do not involve direct interaction of TNF with its receptors, but that other proinflammatory mechanisms capable of up-regulating TNFRI expression may cause cellular activation through the NF-B signaling pathway.Tumor necrosis factor receptor-associated periodic syndrome (TRAPS; MIM no. 142680) is a dominantly inherited chronic inflammatory disorder caused by mutations in the extracellular domains of tumor necrosis factor receptor I (TNFRI), the gene for which is TNFRSF1A (1), and characterized by recurrent fevers and abdominal pain. The most common mutations involve cysteine residues, but several variants involving other residues have also been reported (1,2). More than 30 different pathogenic TNFRSF1A mutations have now been identified (see http://fmf.igh.cnrs.fr/infevers/ and ref.2), mostly located in either the first or second cysteine-rich N-terminal extracellular domain (CRD1 or CRD2) of TNFRSF1A (2,3). Impaired cleavage of the TNFRI (p55) ectodomain upon cellular activation has been demonstrated as a pathogenic mechanism in some but not all TNFRI variants (3-6) and did not relate to the severity of the phenotype (7,8).Biologic activities of TNF are mediated through 2 TNFRs, TNFRI and TNFRII (TNFR superfamily 1B

show abstract

Toxoplasma gondii infection can regulate the expression of tumour necorsis factor‐α receptors on human cell in vitro

Cited by 24 publications

References 49 publications

Inhibition of the Growth ofToxoplasma gondiiin Immature Human Dendritic Cells Is Dependent on the Expression of TNF-α Receptor 2

Inhibition of the Growth ofToxoplasma gondiiin Immature Human Dendritic Cells Is Dependent on the Expression of TNF-α Receptor 2

Activation of NF-κB byToxoplasma gondiicorrelates with increased expression of antiapoptotic genes and localization of phosphorylated IκB to the parasitophorous vacuole membrane

Tumor necrosis factor receptor I from patients with tumor necrosis factor receptor–associated periodic syndrome interacts with wild‐type tumor necrosis factor receptor I and induces ligand‐independent NF‐κB activation

Contact Info

Product

Resources

About