Natural killer T cells ameliorate antibody-induced arthritis in macrophage migration inhibitory factor transgenic mice

Takagi, Dai; Iwabuchi, Kazuya; Maeda, Masanori; Nakamaru, Yuji; Furuta, Yasushi; Fukuda, Satoshi; Kaer, Luc Van; Nishihira, Jun; Onoé, Kazunori

doi:10.3892/ijmm.18.5.829

Cited by 4 publications

(5 citation statements)

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“…As NKT cells can play diverse roles in different experimental models of disease, i.e. as immune-regulatory [8][9][10][11]34] or -enhancing cells [7,14,15,35], the impact of the HFD on NKT cell functions might differ for individual diseases investigated. Furthermore, when treating patients with certain diseases in which NKT cells are involved in the pathogenesis, it may be important to precisely examine the lipid metabolism prior to therapy.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, it has been reported that NKT cells are involved in various autoimmune, inflammatory and allergic diseases, as well as in the host defence that is induced by the acquired immune system [1,2,[5][6][7]. Successful treatments for autoimmune diseases and metastatic cancers in mice have been achieved by activating NKT cells [8][9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

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Effect of High Fat Diet on NKT Cell Function and NKT Cell‐mediated Regulation of Th1 Responses

et al. 2008

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Diet is one of the important factors that modulate immune responses. In the present study, we have examined the capacity of dietary lipids to modify immune responses in mice and we have investigated the contribution of glycolipid‐reactive natural killer T (NKT) cells in this process. Mice fed, high fat diet (HFD; 21.2% fat, 0.20% cholesterol) for 3 weeks, as compared with mice fed standard fat diet (SFD; 4.3% fat, 0.03% cholesterol), showed significantly reduced interferon‐γ production in sera at 6 or 12 h after intraperitoneal injection of an NKT cell ligand, α‐galactosylceramide. In contrast, production of interleukin‐13 was significantly higher at 2 and 6 h in HFD fed mice compared with mice on SFD. No difference was detected in the serum interleukin‐4 levels between these two groups of animals. The proportion of NKT cells in spleen and liver was reduced in mice fed HFD compared with those on SFD. In addition, activation of NKT cells assessed by up‐regulation of CD69 was suppressed specifically in liver from mice fed HFD. Recall responses of conventional T cells and delayed‐type hypersensitivity (Th1 type) against ovalbumin were significantly suppressed in mice fed HFD in comparison with those fed SFD. This suppression was not observed in CD1d−/− mice, suggesting that NKT cells in mice fed HFD played a role in suppressing Th1 responses. Taken together, our findings suggest a critical link between NKT cells, dietary lipid and adaptive immune responses.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of High Fat Diet on NKT Cell Function and NKT Cell‐mediated Regulation of Th1 Responses

et al. 2008

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“…They did not examine the effects of MIF on cell migration, particularly that of NKT cells. Takagi et al (42) reported that Ab-induced arthritis in MIFtransgenic mice is more aggravating than that in wild-type mice. In their study, a-galactosylceramide may have stimulated NKT cells in spleen to trigger immunomodulation against arthritis by promoting Th2-biased immune deviation.…”

Section: Discussionmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor Triggers Chemotaxis of CD74+CXCR2+ NKT Cells in Chemically Induced IFN-γ–Mediated Skin Inflammation

Hsieh

Chen

Lin

et al. 2014

The Journal of Immunology

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IFN-γ mediates chemically induced skin inflammation; however, the mechanism by which IFN-γ–producing cells are recruited to the sites of inflammation remains undefined. Secretion of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, from damaged cells may promote immune cell recruitment. We hypothesized that MIF triggers an initial step in the chemotaxis of IFN-γ–producing cells in chemically induced skin inflammation. Using acute and chronic models of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was examined, and its role in this process was investigated pharmacologically. The cell populations targeted by MIF, their receptor expression patterns, and the effects of MIF on cell migration were examined. TPA directly caused cytotoxicity accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocytic HaCaT cells. Treatment with the MIF antagonist (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester considerably attenuated TPA-induced ear swelling, leukocyte infiltration, epidermal cell proliferation, and dermal angiogenesis. Inhibition of MIF greatly diminished the dermal infiltration of IFN-γ+ NKT cells, whereas the addition of exogenous TPA and MIF to NKT cells promoted their IFN-γ production and migration, respectively. MIF specifically triggered the chemotaxis of NKT cells via CD74 and CXCR2, and the resulting depletion of NKT cells abolished TPA-induced skin inflammation. In TPA-induced skin inflammation, MIF is released from damaged keratinocytes and then triggers the chemotaxis of CD74+CXCR2+ NKT cells for IFN-γ production.

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“…In the absence of MIF, reduced synoviocyte proliferation and increased apoptosis were observed, and this was associated with an increase in synovial p53 expression. Ichiyama et al confirmed that MIF is important in mediating inflammation and joint destruction in collagen-induced arthritis [24], and MIF over-expression in a transgenic model was associated with more severe arthritis [25].…”

Section: Mif Is a Pro-inflammatory Mediator In A Range Of Immune-medimentioning

confidence: 98%

Macrophage Migration Inhibitory Factor: A Therapeutic Target Across Inflammatory Diseases

Hoi¹,

Iskander²,

Morand

2007

IADT

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Macrophage migration inhibitory factor (MIF), a cytokine originally reported in the 1960s as the prototypic T lymphokine, has emerged in recent years as a key factor regulating inflammatory responses. Both by directly activating immune cells, and by participating in activation entrained by other stimuli, MIF is important in innate and adaptive immune responses as well as tissue-specific mechanisms of damage. As a consequence of its involvement in multiple stages of the immune-inflammatory response, MIF has the potential to be involved in the pathogenesis of a range of immune-mediated inflammatory diseases affecting multiple organ systems. Diseases in which a role for MIF has been strongly validated include rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, atherosclerosis, asthma, inflammatory liver disease, and most recently systemic lupus erythematosus. Recent data have provided mechanisms of action for MIF which further support its suitability as a therapeutic target. Finally, MIF has a unique relationship with glucocorticoids, acting to counter-regulate their anti-inflammatory effects, such that MIF antagonist therapy may be a direct route to 'steroid-sparing'. Methods of targeting MIF therapeutically have also emerged in recent years, based on the unique protein structure of MIF which affords opportunities for direct antagonism by small molecules, as well as by protein therapeutics such as monoclonal antibodies. Clinical trials of MIF antagonist therapies are likely before the end of the current decade.

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Natural killer T cells ameliorate antibody-induced arthritis in macrophage migration inhibitory factor transgenic mice

Cited by 4 publications

References 35 publications

Effect of High Fat Diet on NKT Cell Function and NKT Cell‐mediated Regulation of Th1 Responses

Effect of High Fat Diet on NKT Cell Function and NKT Cell‐mediated Regulation of Th1 Responses

Macrophage Migration Inhibitory Factor Triggers Chemotaxis of CD74+CXCR2+ NKT Cells in Chemically Induced IFN-γ–Mediated Skin Inflammation

Macrophage Migration Inhibitory Factor: A Therapeutic Target Across Inflammatory Diseases

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