TNFRp55 controls regulatory T cell responses in <i>Yersinia</i>‐induced reactive arthritis

Cargnelutti, Ethelina; Arias, José L.; Valdéz, Susana R.; Rabinovich, Gabriel A.; Genaro, María Silvia Di

doi:10.1038/icb.2012.65

Cited by 8 publications

(11 citation statements)

References 38 publications

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“…Recently, we reported that TNFRp55 modulates macrophage functions in response to Yersinia LPS stimulation suggesting an essential regulatory role of TNF via TNFRp55 signaling [93]. Furthermore, we have reported that this pathway controlled the induction and function of Treg cells through differential regulation of cytokine production [69]. Our data support the concept that TNFRp55 signaling may participate in the modulation of immune response in ReA, suggesting caution in the use of TNF blockers in cases of chronic ReA.…”

Section: Treatmentsupporting

confidence: 81%

“…In line with these results, we detected higher IL-17 and IFN-γ levels in regional lymph nodes of TNFRp55 −/− mice with Y. enterocolitica-induced ReA and significantly increased number of CD4 + IL-17 + cells in these mice compared to their counterpart wild-type [68]. In addition, in this animal model we observed decreased amounts of IL-10 and Treg cells at arthritis onset (day 14 after infection) in contrast with chronic stage of arthritis [69]. These works and others advocate the idea that in ReA, a specific cellular immune response take place in the joint and chronic stimuli allows to the cells maintain the inflammatory process for long periods [70].…”

Section: (1) Pathogenic Bacteria Attach and Invade The Intestinal Episupporting

confidence: 47%

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Reactive Arthritis: From Clinical Features to Pathogenesis

Cargnelutti¹,

Genaro²

2013

IJCM

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Reactive arthritis (ReA) is a sterile synovitis which occurs after a gastrointestinal or urogenital infection. ReA belongs to Spondyloarthritis (SpA), a group of diseases that share several clinical and radiological features including familiar clustering, absence of rheumatoid factor and association with HLA-B27. Clinically, ReA is characterized by an asymmetric arthritis predominantly affecting the lower limbs, often associated with urethritis, conjunctivitis and other extraarticular symptoms. The ReA prevalence depends on the incidence of causative pathogens. The ReA diagnosis is based on clinical features and serological tests to evidence previous infection. Different treatment including antibiotics, disease modifying antirheumatic drugs (DMARs) and biologic agents has been recommended. Even though knowing that infections trigger the joint inflammation, the ReA pathogenesis remains to be poorly understood. Several animal models and in vitro studies have been used to elucidate the mechanisms involved in ReA development. In this sense, HLA-B27 transgenic rat or mice have been used to explain the role of this molecule in SpA aetiopathogenesis. Moreover, the infectious model of Yersinia-induced ReA in rodents has shed some lights on the relationship between host genetic susceptibility to infection and abnormal immune response in ReA development. Understanding the immune mediators triggering ReA will contribute to find a specific treatment for this arthritis. In this review, we focus on clinical features, epidemiology, treatment, and the different attempts to understand the pathogenesis of ReA.

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Section: Treatmentsupporting

confidence: 81%

Section: (1) Pathogenic Bacteria Attach and Invade The Intestinal Episupporting

confidence: 47%

Reactive Arthritis: From Clinical Features to Pathogenesis

Cargnelutti¹,

Genaro²

2013

IJCM

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“…Previous studies have indicated that neutralization of TNF during rheumatoid arthritis treatment elicited a significant population of Tregs. And the ablation of p55TNF in reactive arthritis mice resulted in a reduced Tregs number and activity indicate that TNF signaling through p55TNFR and p75TNFR is important to the regulation of Treg cell function6869. Another possible mechanism associated with defective T cell responses might be that sustained p55TNFR signaling induces T cell exhaustion.…”

Section: Discussionmentioning

confidence: 99%

Persistent p55TNFR expression impairs T cell responses during chronic tuberculosis and promotes reactivation

Dambuza

Keeton

Hsu

et al. 2016

Sci Rep

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The pleiotropic activities of TNF are mediated by two structurally related but functionally distinct type I transmembrane receptors, p55TNFR and p75TNFR expressed in most cell types, that can be cleaved and act as TNF scavengers. Here, we investigated the effect of persistent p55TNFR cell surface expression during aerosol inhalation challenge with virulent M. tuberculosis H37Rv. We demonstrated that persistency of p55TNFR in macrophage cultures increased the synthesis of soluble TNF, p75TNFR and NO, however, had no effects on bacteria killing ability. Furthermore, it did not facilitate enhanced protection to primary acute M. tuberculosis infection in p55∆NS mice. Without exacerbated lung inflammation, we found a compensatory increase in p75TNFR shedding and decrease in bioactive TNF in BAL of p55∆NS mice after M. tuberculosis challenge. Defective expressions of CD44 and INFγ attributed to an impaired T cell response during persistent p55TNFR expression that caused marginal transient susceptibility during chronic infection. Moreover, persistent p55TNFR expression induced early reactivation during latent tuberculosis infection. These data indicate a prominent role of p55TNFR shedding in Th1 mediated protection against chronic and latent tuberculosis infection.

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“…Yersinia enterocolitica was confirmed as a pathogen of Yersinia and it has been shown that it can also produce Yersinia pseudotuberculosis-derived mitogen, a super antigen that is associated with ReA [33]. A later article [34] revealed the involvement of p40, a common subunit of heterodimeric IL-12 and IL-23, in increasing both IFN-γ and IL-17 production under TNFR p55 deficiency. Taken together, these data indicate that, in the absence of TNFR p55 signaling, Th1 and Th17 effector cells may have a critical function that sustains the inflammatory response in ReA processes.…”

Section: Pathogenesis Of Reamentioning

confidence: 99%

“…IV, Lactobacillus casei can inhibit the expression of TNF-α, IL-17, IL-23, IL-1 and IL-6 in intestinal lymph nodes which lead to protective role in ReA. V, TNFRp55 regulates the cytokine production and enhanced the production of IFN-γ and IL-17, which developed severe chronic Yersinia enterocolitica-induced (ReA) [32][33][34]. (Chlamydia trachomatis) infection is the most common factor causing ReA, which can persist in the host and cause typical reactive arthritis [2].…”

Section: Pathogenesis Of Reamentioning

confidence: 99%

Treatment of reactive arthritis with biological agents: a review

Zeng¹,

Luo²,

Zhang³

et al. 2020

Bioscience Reports

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The pathogenesis of reactive arthritis (ReA) has not been fully elucidated. In recent years, many researchers have confirmed that multiple cytokines are involved in the occurrence and development of ReA. Although ReA is self-limiting, it is still incurable for some patients who have no or a weak response to traditional drugs, such as non-steroidal anti-inflammatory agents, glucocorticoids and immunosuppressive agents. This is called refractory reactive arthritis. Currently, there is insufficient evidences for the treatment of refractory ReA with biological agents, though biological agents against cytokines have been developed over the past few years. This review summarizes the current development of clinical treatments of ReA with biological agents, which provides future investigations on refractory ReA with more evidence and references.

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TNFRp55 controls regulatory T cell responses in Yersinia‐induced reactive arthritis

Cited by 8 publications

References 38 publications

Reactive Arthritis: From Clinical Features to Pathogenesis

Reactive Arthritis: From Clinical Features to Pathogenesis

Persistent p55TNFR expression impairs T cell responses during chronic tuberculosis and promotes reactivation

Treatment of reactive arthritis with biological agents: a review

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