Detection of Macrophage Migration Inhibitory Factor by Monoclonal Antibody in Sézary Syndrome

Neumann, Christine; Schlegel, Renate; Steckel, F.; Sorg, Clemens

doi:10.1111/1523-1747.ep12470326

Cited by 8 publications

(3 citation statements)

References 21 publications

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“…MIF activity was identified during the leukaemic phase of cutaneous T‐cell lymphomas (52). In the cutaneous T‐cell lymphoma Sézary syndrome, MIF was shown to be strongly expressed in skin and blood lymphocytes (53). MIF contributes to the migratory and proliferative functions of human melanoma cells, as well as the neovascularization of G361 melanoma cell‐induced tumors (30).…”

Section: Mif and Cutaneous Pathologiesmentioning

confidence: 99%

MIF: a key player in cutaneous biology and wound healing

Gilliver

Emmerson

Bernhagen

et al. 2010

Experimental Dermatology

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Owing to its implication in a range of pathological conditions, including asthma, rheumatoid arthritis, atherosclerosis, inflammatory bowel disease and cancer, the pleiotropic cytokine macrophage migration inhibitory factor (MIF) has been the subject of intensive recent investigation. In the field of dermatology, MIF is believed to be a detrimental factor in diseases such as systemic sclerosis, atopic dermatitis, psoriasis, eczema and UV radiation damage. However, its contribution to other aspects of cutaneous biology is currently unclear. Although its expression in intact skin is well characterized, little is known about MIF's role in cutaneous homoeostasis. However, recent data do identify MIF as a key player in the immune privilege of hair follicles. Similarly, although MIF is rapidly released and its local expression significantly induced upon wounding, its primary role in the ensuing repair process remains a source of contention. MIF has been identified as being a key effector of the beneficial effects of estrogen on wound repair, yet studies employing Mif null mice, recombinant MIF, and neutralizing anti-MIF antibodies have failed to provide a consensus as to whether it benefits or inhibits healing. In fact MIF appears to be able to exert both positive and negative effects, with the cell-specific relevancy of MIF in wound healing still unclear. Thus, if MIF and ⁄ or its downstream targets are to be therapeutically useful in the context of cutaneous repair, more needs to be done to establish the nature and mechanism of action of MIF and its receptors in healing wounds.

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Section: Mif and Cutaneous Pathologiesmentioning

confidence: 99%

MIF: a key player in cutaneous biology and wound healing

Gilliver

Emmerson

Bernhagen

et al. 2010

Experimental Dermatology

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“…Using the monoclonal antibody 1C5/B against MIF, Neumann et al (Neumann et al 1987) were able to demonstrate immunoreactivity for MIF in peripheral blood lymphocytes (mainly T-helper cells) and skin-infiltrating lymphocytes in a patient with Seza´ry syndrome. In the present study, Seza´ry syndrome patients were not included and only two (nos.…”

Section: Discussionmentioning

confidence: 99%

Galectin fingerprinting by immuno- and lectin histochemistry in cutaneous lymphoma

Wollina

Graefe

Feldrappe

et al. 2002

Journal of Cancer Research and Clinical Oncology

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Owing to their relevance for growth regulation and cell adhesion monitoring the expression of galectins (endogenous beta-galactoside-binding lectins) and their binding sites has relevance for tumor biology. Using galectin-type-specific reagents (non-crossreactive antibodies for proto-type galectin-1, chimera-type galectin-3 and tandem-repeat-type galectins-4 and -8, and labeled galectins-1, -3, and -4) we determined galectin expression in cutaneous T cell lymphomas (CTCL) and controls. In addition to commonly studied galectins-1 and -3, tandem-repeat-type galectins could be detected, i.e., galectin-8 in six from 15 cases and galectin-4 in one of 15 cases. In view of relevant ligands such as bcl-2 or integrins the presence of galectins-3 and -8 seems to be possibly related to loss of proliferation control and change in cell adhesion properties that are involved in clonal expansion and epidermal spread of malignant T cell clones. Successful chemotherapy of CTCL alters galectin expression selectively as shown for liposomal doxorubicin.

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“…The sequence of MRP8 cDNA contains an additional G residue in position 292, which shifts the reading frame of the last 15 amino acids. MRP8 is also referred by other names such as L1 light chain antigen, p8 and calgranulin A, and MRP14, correspondingly, as L1 heavy chain antigen, p14, and calgranulin B [12][13][14]. The protein complex formed by the two S100 proteins is referred by S100A8/A9 or calprotectin.…”

Section: Introductionmentioning

confidence: 99%

Induction of Apoptotic Cell Death in Tumor Cells by S100A8/A9 Released from Inflammatory Cells Upon Cellular Activation

Ghavami¹

2005

CMCAIAA

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Polymorphonuclear neutrophils (PMNs) have received less attention than other leukocyte subsets as potential mediators of antitumor effects. However, there is a growing body of evidence that PMNs are potential mediators of antitumor effects and play an important role in the antitumor response. A protein complex S100A8/A9, formed by the two low molecular weight calcium-binding proteins S100A8 and S100A9, is released from activated PMNs and has apoptosis/cytotoxicity-inducing activity against tumor cell lines. In this review, we focus on the molecular mechanisms by which S100A8/A9 induces apoptosis. Recent studies point to a yet undefined mechanism, probably relaying on cell surface receptor(s), by which S100A8/A9 induces apoptosis in carcinoma cell lines, in addition to zinc exclusion from target cells. Although a number of putative receptors have been identified, the cell-membrane bindings site(s) involved in the apoptosis-inducing activity of S100A8/A9 remain unknown. The identification of the binding site(s) together with the elucidation of the underlying molecular mechanisms will give new insights in how the adaptive immune system is involved in cancer regression.

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Detection of Macrophage Migration Inhibitory Factor by Monoclonal Antibody in Sézary Syndrome

Cited by 8 publications

References 21 publications

MIF: a key player in cutaneous biology and wound healing

MIF: a key player in cutaneous biology and wound healing

Galectin fingerprinting by immuno- and lectin histochemistry in cutaneous lymphoma

Induction of Apoptotic Cell Death in Tumor Cells by S100A8/A9 Released from Inflammatory Cells Upon Cellular Activation

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