Becker H, Maaser C, Mickholz E, et al. Relationship between serum levels of macrophage migration inhibitory factor and the activity of antineutrophil cytoplasmic antibody-associated vasculitides

Department of Medicine B, University of Muenster, Albert-Schweitzer-Strasse 33, 48129 Münster, Germany.
Clinical Rheumatology (Impact Factor: 1.7). 05/2006; 25(3):368-72. DOI: 10.1007/s10067-005-0045-9
Source: PubMed


Macrophage migration inhibitory factor (MIF) is a central proinflammatory cytokine that regulates innate and adaptive immune responses. To evaluate its role in primary vasculitides, we determined MIF by enzyme-linked immunoassay in the sera of patients with Wegener's granulomatosis (WG; n=26), microscopic polyangiitis (MPA; n=10), polyarteritis nodosa (PAN; n=9) and giant cell arteritis (GCA; n=11). Healthy controls (n=26) and patients with sarcoidosis (n=14) were studied in parallel. Serum levels of MIF were significantly higher in patients with WG (median 41.1, range 3.2-120 ng/ml) than those in healthy controls (6.0, 0.015-36.5 ng/ml; P<0.001) and in patients with sarcoidosis (13.8, 0.015-67.1 ng/ml; P<0.05). MIF values were higher in MPA patients (29.5, 9.9-69.4 ng/ml; P<0.01) in comparison with those in healthy controls. In particular, increased levels of MIF were associated with active disease as assessed by the Birmingham Vasculitis Activity Score. Sequential studies showed decreased levels of MIF after initiation of immunosuppressive therapy, with clinical improvement in WG and MPA patients. In contrast, serum levels of MIF were not significantly elevated in patients with PAN and GCA. The results suggest that MIF contributes to the inflammatory process and correlates with disease activity in antineutrophil cytoplasmic antibody-associated vasculitides.

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    • "Furthermore, MIF levels were significantly diminished in MPA patients exhibiting clinical improvement after treatment. Similarly, serum MIF levels were elevated in patients with antineutrophil cytoplasmic antibody- (ANCA-) related vasculitis [95], as well as in Wegener's granulomatous and Kawasaki disease [96]. These findings indicate that MIF expression is not specific to RA, but may also function as an important regulator of systemic vasculitis. "
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    ABSTRACT: Macrophage migration inhibitory factor (MIF) was originally identified in the culture medium of activated T lymphocytes as a soluble factor that inhibited the random migration of macrophages. MIF is now recognized to be a multipotent cytokine involved in the regulation of immune and inflammatory responses. Moreover, the pivotal nature of its involvement highlights the importance of MIF to the pathogenesis of various inflammatory disorders and suggests that blocking MIF may be a useful therapeutic strategy for treating these diseases. This paper discusses the function and expressional regulation of MIF in several rheumatic diseases and related conditions.
    12/2010; 2010(2090-1984):106202. DOI:10.1155/2010/106202
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    • "There is increasing evidence for a role of MIF as a proinflammatory cytokine in autoimmune diseases [6]. Serum levels of MIF have been shown to be correlated with the disease activity in several autoimmune disorders including juvenile idiopathic arthritis, rheumatoid arthritis and Wegener's granulomatosis [7-9]. Foote and colleagues [10] recently reported increased MIF levels and a correlation with the disease activity in patients with systemic lupus erythematosus. "
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    ABSTRACT: The objective of this study was to analyse levels of the proinflammatory cytokine macrophage migration inhibitory factor (MIF) in patients with primary Sjögren's syndrome (pSS) and to examine associations of MIF with clinical, serological and immunological variables. MIF was determined by ELISA in the sera of 76 patients with pSS. Further relevant cytokines (IL-1, IL-6, IL-10, IFN-gamma and TNF-alpha) secreted by peripheral blood mononuclear cells (PBMC) were determined by ELISPOT assay. Lymphocytes and monocytes were examined flow-cytometrically for the expression of activation markers. Results were correlated with clinical and laboratory findings as well as with the HLA-DR genotype. Healthy age- and sex-matched volunteers served as controls. We found that MIF was increased in patients with pSS compared with healthy controls (p < 0.01). In particular, increased levels of MIF were associated with hypergammaglobulinemia. Further, we found a negative correlation of MIF levels with the number of IL-10-secreting PBMC in pSS patients (r = -0.389, p < 0.01). Our data indicate that MIF might participate in the pathogenesis of primary Sjögren's syndrome. MIF may contribute to B-cell hyperactivity indicated by hypergammaglobulinemia. The inverse relationship of IL-10 and MIF suggests that IL-10 works as an antagonist of MIF in pSS.
    Arthritis research & therapy 02/2007; 9(2):R43. DOI:10.1186/ar2182 · 3.75 Impact Factor
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    ABSTRACT: Giant cell arteritis and Takayasu arteritis are well known large vessel vasculitides with an unknown etiology. As they have similar clinical features, this short article reviews recent advances in clinical and pathophysiological findings, focusing in particular on papers published in the past year. Delayed gadolinium-enhanced magnetic resonance imaging showed delayed hyperenhancement in the aortic wall in Takayasu arteritis. This technique may be useful in monitoring disease activity or inflammation in the arterial wall and can be used for small vessels such as temporal arteries in giant cell arteritis with high-resolution imaging. Evidence is accumulating that antitumor necrosis factor-alpha monoclonal antibody therapy can be useful for patients refractory to corticosteroid and/or immunosuppressant treatment. Functional promoter polymorphisms of genes encoding inducible nitric oxide synthase and I-kappaB-like protein were suggested to be associated with susceptibility to giant cell arteritis and Takayasu arteritis, respectively. Advances in imaging technique will make it possible to evaluate inflammatory activity of the vascular lesions and provide a useful guide for treatment of giant cell arteritis and Takayasu arteritis. Further understanding of the pathophysiological mechanism may contribute to the development of new medicine targeting critical factors in the pathogenesis, such as antitumor necrosis factor-alpha agents.
    Current Opinion in Rheumatology 02/2007; 19(1):39-43. DOI:10.1097/BOR.0b013e3280119866 · 4.89 Impact Factor
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