High levels of natural killer cells are associated with response to tocilizumab in patients with severe rheumatoid arthritis

Daïen, C.; Gailhac, Sarah; Audo, Rachel; Mura, Thibault; Hahne, Michael; Combe, Bernard; Morel, Jacques

doi:10.1093/rheumatology/keu363

Cited by 41 publications

(36 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…bright phenotype (36)(37)(38)(39). In line with this, patients with psoriasis show an increase in CD56 bright NK cells in cutaneous lesions (63,64).…”

Section: Cd56 Bright Nk Cells In Tissuessupporting

confidence: 59%

“…NK cells are considered pathogenic elements in the development of the disease (34,35). The proportions of CD56 bright and CD56 dim NK cells in the peripheral blood of RA patients are similar to those in healthy subjects (36)(37)(38)(39). The same observation was made for type 1 diabetes patients, with no significant difference compared with healthy controls (40,41).…”

Section: Cd56mentioning

confidence: 52%

See 1 more Smart Citation

Human CD56bright NK Cells: An Update

Michel

Poli

Cuapio

et al. 2016

The Journal of Immunology

326

273

View full text Add to dashboard Cite

Human NK cells can be subdivided into various subsets based on the relative expression of CD16 and CD56. In particular, CD56brightCD16−/dim NK cells are the focus of interest. They are considered efficient cytokine producers endowed with immunoregulatory properties, but they can also become cytotoxic upon appropriate activation. These cells were shown to play a role in different disease states, such as cancer, autoimmunity, neuroinflammation, and infection. Although their phenotype and functional properties are well known and have been extensively studied, their lineage relationship with other NK cell subsets is not fully defined, nor is their precise hematopoietic origin. In this article, we summarize recent studies about CD56bright NK cells in health and disease and briefly discuss the current controversies surrounding them.

show abstract

“…bright phenotype (36)(37)(38)(39). In line with this, patients with psoriasis show an increase in CD56 bright NK cells in cutaneous lesions (63,64).…”

Section: Cd56 Bright Nk Cells In Tissuessupporting

confidence: 59%

Section: Cd56mentioning

confidence: 52%

Human CD56bright NK Cells: An Update

Michel

Poli

Cuapio

et al. 2016

The Journal of Immunology

326

273

View full text Add to dashboard Cite

show abstract

“…Younger age, high baseline CRP level and no history of prior cardiovascular disease were predictors of better response to tocilizumab therapy [18]. Moreover, genetic variation in the IL-6 receptor [19] and natural killer cell proportion at baseline [20] were predictive factors for tocilizumab response. However, predictors in the early stage after starting tocilizumab treatment have received little attention.…”

Section: Discussionmentioning

confidence: 96%

“…Predicting the effects of tocilizumab therapy at the early stage is thus quite difficult. Some recent studies have investigated predictors of tocilizumab response at baseline [17][18][19][20]. However, predictors in the early stage after starting tocilizumab treatment have not been reported [21].…”

Section: Introductionmentioning

confidence: 99%

Levels of interleukin-1 beta can predict response to tocilizumab therapy in rheumatoid arthritis: the PETITE (predictors of effectiveness of tocilizumab therapy) study

et al. 2015

View full text Add to dashboard Cite

Predicting the responses of patients with rheumatoid arthritis (RA) to tocilizumab is difficult, because inflammatory markers such as C-reactive protein rapidly normalize regardless of clinical efficacy. We aimed to identify factors that could predict response to tocilizumab. Sixty-five patients completed 52 weeks of tocilizumab therapy. Serum fibrinogen, D-dimer and interleukin (IL)-1β levels were measured at baseline and after 4 weeks of therapy. Clinical responses to tocilizumab were assessed using disease activity score 28-erythrocyte sedimentation rate and the clinical disease activity index at baseline and after 52 weeks of therapy (UMIN Clinical Trials Registry No. UMIN000002246). Mean age was 60.5 years (range 22-85 years). Mean disease duration was 11.2 years (range 0-45 years). All patients had moderate-to-severe disease activity and were resistant to disease-modifying anti-rheumatic drugs and/or other biologics. Baseline IL-1β levels were significantly lower in responders than in non-responders (p = 0.045), but multiple logistic regression analysis found no significant difference (adjusted odds ratio 2.74; 95 % confidence interval 0.84-8.95; p = 0.096). Low D-dimer and IL-1β levels at 4 weeks predicted greater decrease in disease activity after 52 weeks of treatment (p = 0.005 and p < 0.001, respectively). Effects of tocilizumab at 52 weeks could be predicted from D-dimer and IL-1β levels after 4 weeks of tocilizumab treatment. These markers might be more useful than current inflammatory markers for early-stage prediction of response to tocilizumab in RA.

show abstract

“…IL-6 overproduction in mouse models in vivo inhibited inducible Foxp3+ Tregs (iTregs) generation from naive T cells [41]. In RA patients, TCZ was found to induce an increased frequency of Tregs after 3-month treatment [42]. Induced Tregs could thus promote induction of a TCZ-specific tolerance.…”

Section: Discussionmentioning

confidence: 99%