T cells are involved in the development of arthritis induced by anti-type II collagen antibody

Mitamura, Mana; Nakano, Nami; Yonekawa, Taeko; Shan, Lihua; Kaise, Toshihiko; Kobayashi, Takao; Yamashita, Koh; Kikkawa, Hideo; Kinoshita, Mine

doi:10.1016/j.intimp.2007.05.021

Cited by 26 publications

(22 citation statements)

References 38 publications

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“…Abatacept is known to inhibit T cell activation and proliferation14 by blocking costimulatory ligands CD80 and CD86 on antigen presenting cells (dendritic cells, B cells and macrophages)39565758. Despite early contrasting data, abatacept has been shown not to act via induction of signals in dendritic cells5960.…”

Section: Discussionmentioning

confidence: 99%

“…Despite early contrasting data, abatacept has been shown not to act via induction of signals in dendritic cells5960. Yet, as it interacts with macrophages and B cells, it is not surprising that it can directly inhibit monocyte/macrophage activation and function3361 and B-cell function34395758. The functions of macrophages and B cells affected by abatacept are related to T cell-dependent responses333439, possibly as these functions involve CD80/CD86.…”

Section: Discussionmentioning

confidence: 99%

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T cell costimulation blockade blunts pressure overload-induced heart failure

et al. 2017

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Heart failure (HF) is a leading cause of mortality. Inflammation is implicated in HF, yet clinical trials targeting pro-inflammatory cytokines in HF were unsuccessful, possibly due to redundant functions of individual cytokines. Searching for better cardiac inflammation targets, here we link T cells with HF development in a mouse model of pathological cardiac hypertrophy and in human HF patients. T cell costimulation blockade, through FDA-approved rheumatoid arthritis drug abatacept, leads to highly significant delay in progression and decreased severity of cardiac dysfunction in the mouse HF model. The therapeutic effect occurs via inhibition of activation and cardiac infiltration of T cells and macrophages, leading to reduced cardiomyocyte death. Abatacept treatment also induces production of anti-inflammatory cytokine interleukin-10 (IL-10). IL-10-deficient mice are refractive to treatment, while protection could be rescued by transfer of IL-10-sufficient B cells. These results suggest that T cell costimulation blockade might be therapeutically exploited to treat HF.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

T cell costimulation blockade blunts pressure overload-induced heart failure

et al. 2017

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“…These results are similar to those seen in the K/BxN model of arthritis with histidine decarboxylase-deficient mice that lack histamine 20. The CAIA and K/BxN transfer model have similar underlying mechanisms and therefore it is reasonable to assume that the effects reported in histidine decarboxylase-deficient mice are due to lack of histamine activation of the H 4 R. Both of these models are thought to be driven by activation of the innate immune system, and T cells are not thought to be involved until later in the disease progression 21. While the exact mechanisms for the role of the H 4 R in the models are not known, transfer of wild-type CD11c + cells can restore the disease in H 4 R-deficient mice, and there is evidence that the receptor can play a role in mast cell, dendritic cell, NK T cell and macrophage activation 7 18 22 23.…”

Section: Discussionmentioning

confidence: 99%

The histamine H₄ receptor mediates inflammation and Th17 responses in preclinical models of arthritis

Cowden

Banie

et al. 2013

Ann Rheum Dis

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ObjectiveThe histamine H4 receptor (H4R) has been shown to drive inflammatory responses in models of asthma, colitis and dermatitis, and in these models it appears to affect both innate and adaptive immune responses. In this study, we used both H4R-deficient mice and a specific H4R antagonist, JNJ 28307474, to investigate the involvement of the H4R in mouse arthritis models.MethodsH4R-deficient mice and wild-type mice administered the H4R antagonist were studied in models of collagen antibody-induced arthritis (CAIA) and collagen-induced arthritis (CIA). The impact on Th17 cells was assessed by restimulation of inguinal lymphocytes in the disease or immunisation models and with in vitro stimulation of whole blood.ResultsBoth H4R-deficient mice and mice treated with the H4R antagonist exhibited reduced arthritis disease severity in both CAIA and CIA models. This was evident from the reduction in disease score and in joint histology. In the CIA model, treatment with the H4R antagonist reduced the number of interleukin (IL)-17 positive cells in the lymph node and the total production of IL-17. Th17 cell development in vivo was reduced in H4R-deficient mice or in mice treated with an H4R antagonist. Finally, treatment of both mouse and human blood with an H4R antagonist reduced the production of IL-17 when cells were stimulated in vitro.ConclusionsThese results implicate the H4R in disease progression in arthritis and in the production of IL-17 from Th17 cells. This work supports future clinical exploration of H4R antagonists for the treatment of rheumatoid arthritis.

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“…In murine models, the effects of certain biologic agents administered early in the induction phases of experimental arthritis prevent the progression of synovitis [16]. Nevertheless, RA is a complex disease unique to humans, and there is currently no single universal agreement upon the definition of early RA.…”

Section: Definition Of Early Rheumatoid Arthritismentioning

confidence: 99%

Biologic therapy for early rheumatoid arthritis: the latest evidence

Castro-Rueda

Kavanaugh

2008

Current Opinion in Rheumatology

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The addition of antitumor necrosis factor-alpha agents to traditional disease-modifying antirheumatic drugs in early rheumatoid arthritis is a novel strategy which follows the principle of early and aggressive therapeutic intervention. Results from recent trials show greater levels of disease control. The impact on long-term safety and cost-efficacy are factors which will need to be better characterized over time.

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T cells are involved in the development of arthritis induced by anti-type II collagen antibody

Cited by 26 publications

References 38 publications

T cell costimulation blockade blunts pressure overload-induced heart failure

T cell costimulation blockade blunts pressure overload-induced heart failure

The histamine H₄ receptor mediates inflammation and Th17 responses in preclinical models of arthritis

Biologic therapy for early rheumatoid arthritis: the latest evidence

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T cells are involved in the development of arthritis induced by anti-type II collagen antibody

Cited by 26 publications

References 38 publications

T cell costimulation blockade blunts pressure overload-induced heart failure

T cell costimulation blockade blunts pressure overload-induced heart failure

The histamine H4 receptor mediates inflammation and Th17 responses in preclinical models of arthritis

Biologic therapy for early rheumatoid arthritis: the latest evidence

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Product

Resources

About

The histamine H₄ receptor mediates inflammation and Th17 responses in preclinical models of arthritis