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Septic shock
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Bryan E. Freeman, Michael R. Foley
Along these same lines, macrophage migration inhibitory factor (MIF) is induced by glucocorticoids in sepsis and is probably involved in sepsis pathogenesis. Experiments in mice have found that inhibition of MIF leads to attenuation of inflammatory mediators such as TNF-α and IL-1β (8).
Immunomodulatory Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
The first cytokine, interferon alpha (a Type-1 interferon), was identified in 1957 as a protein that interfered with viral replication. The activity of interferon gamma (the only member of the interferon Type-2 class) was described in 1965, and it was the first lymphocyte-derived mediator to be identified. Macrophage migration inhibitory factor (MIF) was identified in 1966. In 1969 the term “lymphokine” was proposed to describe proteins secreted from lymphocytes, and proteins derived from macrophages and monocytes in culture were later referred to as “monokines”. As researchers gradually learned more, it was realized that these and related proteins were part of a broader class of proteins involved in self-defence, and so the term “cytokine” was coined as an over-arching name. Although the nomenclature is still confusing in some areas, in general cytokines are now referred to as “immunomodulating agents”. However, most would agree that more work is needed to properly define and name the various families of cytokines and hormones.
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
S100A8 is also called calgranulin A or MRP8. S100A9 is also called calgranulin B or MRP14. At the time of discovery in 1987, they were actually called macrophage migration inhibitory factor (MIF)–related proteins: MRP8 and MRP14 (see Section 5.2.5.20). They preferentially form the S100A8/A9 heterodimer, which is called leukocyte protein L1 or cystic fibrosis antigen or calprotectin. These are abundantly expressed in myeloid cells, for example, neutrophils, monocytes, and early macrophages, and also to some extent in keratinocytes. In inflamed microvasculature, the S100A8/A9 complex is deposited onto the endothelium of venules associated with extravasating leukocytes. Normal tissue macrophages do not express S100A8/A9. Chronic inflammatory macrophages, for example, in RA, sarcoidosis, tuberculosis, or onchocerciasis, express both S100A8 and A9, but macrophages in acute inflammation usually express only S100A9. In neutrophils, the S100A8/A9 complex is the most abundant cytosolic protein and may represent almost 45% (30%–60%) of the soluble cytosolic protein content, and the level is 40-fold less in monocytes. This protein is also present in neutrophil granules, especially secondary granules, but the localization is blurred by the cytosolic abundance. IL10 indirectly and slowly stimulates S100A8/A9 production in a COX2-cAMP-dependent way, whereas Th2 cytokines IL4 and IL13 suppress them. Neutrophilic calprotectin, possibly largely cytosolic, is actively extruded with NETs, and this calprotectin is absolutely necessary for antifungal activity of NET in vitro.
Macrophage Migration Inhibitory Factor - 173 G/C Polymorphism is Associated With The Age of Onset and Insight in Schizophrenia in the Turkish Population
Published in Neurological Research, 2021
Hasan Mervan Aytac, Yasemin Oyaci, Menekse Sila Yazar, Sacide Pehlivan
Macrophage migration inhibitory factor (MIF) is a potent cytokine that plays a vital role in the innate and acquired immune response and is involved in the etiopathogenesis of various autoimmune diseases. The MIF gene is localized to the q11.23 region on chromosome 22. Two functional polymorphisms located in the MIF gene were reported to modulate MIF promoter activity and relate to MIF expression levels: the – 794 CATT5–8 microsatellite repeat and the −173 G/C (rs755622) single nucleotide polymorphism (SNP) [4]. In literature, it was seen that the MIF gene plays an essential role in the pathophysiology of sepsis, acute respiratory distress syndrome, tuberculosis, and diabetes [5]. MIF has also been shown to facilitate the DNA damage response, and cell cycle regulation is related to the hypothalamic-pituitary-adrenal (HPA) axis [6]. When the literature is reviewed, there is no study examining the relationship between MIF −173 G/C polymorphism and SCZ in the Turkish population. To our knowledge, this is the first clinical study comparing MIF −173 G/C distributions in patients with SCZ according to scale scores, treatment resistance, insight in disease, and clinical parameters in detail. This study aimed to investigate the relationship between clinical features of psychiatric disorder and MIF −173 G/C polymorphism in patients with SCZ by comparing genotype distributions of MIF −173 G/C between patients and healthy controls.
Peripheral blood and tissue assessment highlights differential tumor-circulatory gradients of IL2 and MIF with prognostic significance in resectable pancreatic ductal adenocarcinoma
Published in OncoImmunology, 2021
Azaz Ahmed, Sophia Köhler, Rosa Klotz, Nathalia Giese, Felix Lasitschka, Thilo Hackert, Christoph Springfeld, Inka Zörnig, Dirk Jäger, Niels Halama
The identification of reliable parameters for early diagnosis as well as prognosis of PDA is an unmet need and pivotal to improve clinical decision-making and patient outcomes. Cytokines as inflammatory molecules play an important role in the development and progression of PDA, and tumor cell-intrinsic cytokines have the potential to shape local immunity.6,7 Originating from the tumor microenvironment, cytokines orchestrate various pro- and antitumoral functions and thereby potentially qualify as biomarkers for PDA.8 Existing evidence demonstrates that a broad range of cytokines have a diagnostic or prognostic potential.9 But previous data is heterogenous, for example, elevated as well as decreased circulatory interleukin 2 (IL2) levels have both been described as diagnostic markers for disease.9–11 Another cytokine of interest is macrophage migration inhibitory factor (MIF), which is widely secreted by immune and nonimmune cells. MIF exists as a multimeric protein and has multiple functions, including inhibition of T cell activation and alteration of macrophage functionality and differentiation.12,13 Also, tumoral overexpression of MIF has been described in various malignancies (including PDA) being associated with poor prognosis, higher metastatic potential, and higher tumor burden.14–18 However, uncertainty exists regarding the role of circulatory MIF levels and their diagnostic and prognostic value in PDA patients.
Targeted urine proteomics in lupus nephritis – a meta-analysis
Published in Expert Review of Proteomics, 2020
Ting Zhang, Valeria Duran, Kamala Vanarsa, Chandra Mohan
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine with chemokine-like properties [51]. Consistent with results of scRNA-seq analysis of LN kidneys (Figure 2(e)), in a study where MIF expression was examined by in situ hybridization and immunohistochemistry staining, MIF mRNA and protein were constitutively expressed in normal human kidney, and both glomerular and tubular MIF were markedly up-regulated in proliferative glomerulonephritis (GN), including LN. In addition, many infiltrating macrophages and T cells showed MIF expression. MIF expression was significantly correlated with leukocyte infiltration, histologic damage, and renal function impairment, suggesting that MIF may be an important mediator of renal injury in progressive GN [52]. In MRL/lpr mice, renal MIF expression was upregulated compared with control MRL+/+ mice. MIF-deficient MRL/lpr mice exhibited markedly reduced renal damage, and MIF inhibitor mitigated nephritis in NZB/W F1 and MRL/lp mice [53,54]. Urinary MIF was significantly higher in active SLE compared with inactive SLE, and was positively correlated with SLEDAI [53]. In LN patients, urine MIF/Cr ratio differentiated active disease from inactive disease, and correlated with the activity indices of renal pathology [55]. Elevated urinary MIF may originate from upregulated expression of MIF in renal cells, reflecting its pathogenic role and therapeutic potential. However, elevated urinary MIF may not be specific for LN, as it also increased in acute kidney injury [56], pediatric Henoch-Schönlein purpura nephritis [57], and IgA nephropathy [58,59].