Purification, Bioactivity, and Secondary Structure Analysis of Mouse and Human Macrophage Migration Inhibitory Factor (MIF)

Bernhagen, Jürgen; Mitchell, Robert A.; Calandra, Thierry; Voelter, Wolfgang; Cerami, Anthony; Bucala, Richard

doi:10.1021/bi00251a025

Cited by 398 publications

(417 citation statements)

References 48 publications

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“…The macrophage migration inhibitory factor (MIF) was one of the earliest discovered pro-inflammatory cytokines. Its release from intracellular pools in macrophages and T cells results in the production of nitric oxide and TNF-α in an autocrine stimulatory manner (Bernhagen et al 1994). MIF also has been implicated in DTH, as MIFblocking antibodies attenuate the DTH immune response (Bernhagen et al 1996).…”

Section: The Pro-inflammatory Effects Of Gcs Outside the Nervous Systemmentioning

confidence: 99%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

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In recent years the classic view that glucocorticoids, the adrenal steroids secreted during stress, are universally anti-inflammatory has been challenged at a variety of levels. It was first observed that under some circumstances, acute GC exposure could have pro-inflammatory effects on the peripheral immune response. More recently, chronic exposure to GCs has been found to have pro-inflammatory effects on the specialized immune response to injury in the central nervous system. Here we review the evidence that in some cases, glucocorticoids can increase pro-inflammatory cell migration, cytokine production, and even transcription factor activity in the brain. We consider how these unexpected effects of glucocorticoids can co-exist with their well-established anti-inflammatory properties, as well as the considerable clinical implications of these findings.

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Section: The Pro-inflammatory Effects Of Gcs Outside the Nervous Systemmentioning

confidence: 99%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

View full text Add to dashboard Cite

show abstract

“…MIF was one of the first cytokines described, and is secreted by activated T cells, macrophages, and a variety of nonimmune cells (7)(8)(9)(10). MIF was recently cloned and shown to have a plethora of immunologic activities, including the inhibition of migration and enhanced TNF-␣ and NO production by macrophages (11,12). Furthermore, it regulates T cell activation and proliferation (13).…”

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

In Vivo Blockade of Macrophage Migration Inhibitory Factor Ameliorates Acute Experimental Autoimmune Encephalomyelitis by Impairing the Homing of Encephalitogenic T Cells to the Central Nervous System

Denkinger

Kort

et al. 2003

The Journal of Immunology

102

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Macrophage migration inhibitory factor (MIF) is a cytokine that plays a critical role in the regulation of macrophage effector functions and T cell activation. However, its role in the pathogenesis of T cell-mediated autoimmune diseases, such as experimental autoimmune encephalomyelitis (EAE), has remained unresolved. In this study, we report that anti-MIF Ab treatment of SJL mice with acute EAE improved the disease severity and accelerated the recovery. Furthermore, the anti-MIF treatment impaired the homing of neuroantigen-reactive pathogenic T cells to the CNS in a VCAM-1-dependent fashion. Interestingly, MIF blockade also decreased the clonal size of the neuroantigen-specific Th1 cells and increased their activation threshold. Taken together, the results demonstrate an important role for MIF in the pathogenesis of EAE/multiple sclerosis and suggest that MIF blockade may be a promising new strategy for the treatment of multiple sclerosis.

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“…Macrophages secrete MIF following treatment with pro-inflammatory stimuli, including lipopolysaccharide (LPS), TNF (tumor necrosis factor) and IFNG (interferon, gamma), 7 and it can act in an autocrine or paracrine manner to stimulate the release of other pro-inflammatory mediators, enhance phagocytosis and increase production of reactive oxygen species (ROS) and nitric oxide (NO). [7][8][9][10] MIF has been demonstrated to be an important protective factor in the immune response to Gramnegative bacteria, including Escherichia coli and Klebsiella pneumonia. 11 However, hypersecretion of MIF is associated with pathogenesis in a number of autoimmune conditions, including rheumatoid arthritis, atherosclerosis and systemic lupus erythematosus.…”

Section: Introductionmentioning

confidence: 99%

Loss of autophagy enhances MIF/macrophage migration inhibitory factor release by macrophages

et al. 2016

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MIF (macrophage migration inhibitory factor [glycosylation-inhibiting factor]) is a pro-inflammatory cytokine expressed in multiple cells types, including macrophages. MIF plays a pathogenic role in a number of inflammatory diseases and has been linked to tumor progression in some cancers. Previous work has demonstrated that loss of autophagy in macrophages enhances secretion of IL1 family cytokines. Here, we demonstrate that loss of autophagy, by pharmacological inhibition or siRNA silencing of Atg5, enhances MIF secretion by monocytes and macrophages. We further demonstrate that this is dependent on mitochondrial reactive oxygen species (ROS). Induction of autophagy with MTOR inhibitors had no effect on MIF secretion, but amino acid starvation increased secretion. This was unaffected by Atg5 siRNA but was again dependent on mitochondrial ROS. Our data demonstrate that autophagic regulation of mitochondrial ROS plays a pivotal role in the regulation of inflammatory cytokine secretion in macrophages, with potential implications for the pathogenesis of inflammatory diseases and cancers.

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Purification, Bioactivity, and Secondary Structure Analysis of Mouse and Human Macrophage Migration Inhibitory Factor (MIF)

Cited by 398 publications

References 48 publications

An inflammatory review of glucocorticoid actions in the CNS

An inflammatory review of glucocorticoid actions in the CNS

In Vivo Blockade of Macrophage Migration Inhibitory Factor Ameliorates Acute Experimental Autoimmune Encephalomyelitis by Impairing the Homing of Encephalitogenic T Cells to the Central Nervous System

Loss of autophagy enhances MIF/macrophage migration inhibitory factor release by macrophages

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