Intracellular detection of macrophage migration inhibitory factor in peripheral blood leukocytes

Lehmann, Lutz; Weber, Stefan; Fuchs, D.; Klaschik, Sven; Schewe, J.-C.; Book, Malte; Hoeft, Andreas; Stüber, Frank

doi:10.1016/j.freeradbiomed.2004.12.029

Cited by 14 publications

(12 citation statements)

References 51 publications

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“…Unlike other cytokines, abundant preformed and renewable stores of MIF are present in multiple immune and nonimmune cell types (4,16,(31)(32)(33). Constitutively expressed MIF has immunoregulatory functions in sepsis, inflammatory diseases, and tumorigenesis (4,12,13,34,35).…”

Section: Discussionmentioning

confidence: 99%

Regulation of IL-1 and TNF Receptor Expression and Function by Endogenous Macrophage Migration Inhibitory Factor

Toh

Aeberli

Lacey

et al. 2006

The Journal of Immunology

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Macrophage migration inhibitory factor (MIF) has a key role in regulation of innate and adaptive immunity and is implicated in sepsis, tumorigenesis, and autoimmune disease. MIF deficiency or immunoneutralization leads to protection against fatal endotoxic, exotoxic, and infective shock, and anti-inflammatory effects in other experimental models of inflammatory disease. We report a novel regulatory role of MIF in type 1 IL-1R and p55 TNFR expression and function. Compared with wild-type cells, MIF-deficient cells were hyporesponsive to IL-1- and TNF-induced MAPK activity, AP-1 activity, and cellular proliferation, while NF-κB function was preserved. Hyporesponsiveness of MIF-deficient cells was associated with down-regulation of cytokine receptor expression, which was restored by reconstitution of either an upstream kinase of MAPK, MAPK/ERK kinase, or MIF. These data suggest that endogenous MIF is required for cytokine activation of MAPK/AP-1 and cytokine receptor expression. This autocrine regulatory pathway defines an important amplifying role of endogenous MIF in cytokine-mediated immune and inflammatory diseases and provides further molecular evidence for the critical role of MIF in cellular activation.

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Section: Discussionmentioning

confidence: 99%

Regulation of IL-1 and TNF Receptor Expression and Function by Endogenous Macrophage Migration Inhibitory Factor

Toh

Aeberli

Lacey

et al. 2006

The Journal of Immunology

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“…Given the wide range of cytokines carried by the PMVs, we decided to focus on TGF-b1, which if present on the surface of released PMVs, we surmised, could potentially bind in an autocrine/paracrine-like manner to its cognate receptor on myeloid cells and initiate differentiation. Since TGF-b1 has a signal peptide, we also examined whether cytokines, such as MIF, FGF-1, and Gal-3, which lack a signal sequence (28)(29)(30), are transported in PMVs. Although it has previously been shown that such leaderless cytokines are transported via a nonconventional secretory process (6, 7), note that most of these studies are based on exosomes, which, unlike PMVs, which are released through a budding process from the cell's plasma membrane, are released upon fusion of multivesicular bodies with the plasma membrane (31).…”

Section: Characterization Of Pmvs Isolated From Thp-1 Monocytesmentioning

confidence: 99%

Human Plasma Membrane-Derived Vesicles Halt Proliferation and Induce Differentiation of THP-1 Acute Monocytic Leukemia Cells

Ansa-Addo

Lange²,

Stratton

et al. 2010

The Journal of Immunology

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Plasma membrane-derived vesicles (PMVs) are small intact vesicles released from the cell surface that play a role in intercellular communication. We have examined the role of PMVs in the terminal differentiation of monocytes. The myeloid-differentiating agents all-trans retinoic acid/PMA and histamine, the inflammatory mediator that inhibits promonocyte proliferation, induced an intracellular Ca2+-mediated PMV (as opposed to exosome) release from THP-1 promonocytes. These PMVs cause THP-1 cells to enter G0–G1 cell cycle arrest and induce terminal monocyte-to-macrophage differentiation. Use of the TGF-β receptor antagonist SB-431542 and anti–TGF-β1 Ab showed that this was due to TGF-β1 carried on PMVs. Although TGF-β1 levels have been shown to increase in cell culture supernatants during macrophage differentiation and dendritic cell maturation, the presence of TGF-β1 in PMVs is yet to be reported. In this study, to our knowledge we show for the first time that TGF-β1 is carried on the surface of PMVs, and we confirm the presence within PMVs of certain leaderless proteins, with reported roles in myeloid cell differentiation. Our in vitro findings support a model in which TGF-β1–bearing PMVs, released from promonocytic leukemia cells (THP-1) or primary peripheral blood monocytes on exposure to sublytic complement or after treatment with a differentiation therapy agent, such as all-trans retinoic acid, significantly reduce proliferation of THP-1 cells. Such PMVs also induce the terminal differentiation of primary peripheral blood monocytes as well as THP-1 monocytes.

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“…By controlling immune and inflammatory responses, MIF is thought to play an important role in the pathophysiology of septic shock and chronic inflammatory diseases [5-7]. The role of MIF mediating HTS restoration of T cell dysfunction is unknown.…”

Section: Introductionmentioning

confidence: 99%

Effect of hypertonic saline and macrophage migration inhibitory factor in restoration of T cell dysfunction

et al. 2011

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PurposeTrauma-induced suppression of cellular immune function likely contributes to sepsis, multiple organ dysfunction syndrome and death. T cell proliferation decreases after traumatic stress. The addition of prostaglandin E2 (PGE2), which depresses immune function after hemorrhage and trauma, to T-cells decreases T-cell proliferation; and hypertonic saline restores PGE2-induced T-cell suppression. Recently, it has become apparent that macrophage migration inhibitory factor (MIF) plays a central role in several immune responses, including T-cell proliferation. However, the role of MIF in mediating hypertonic saline (HTS) restoration of T cell dysfunction is unknown. Therefore, we hypothesize that T cell immune restoration by HTS occurs, at least in part, by a MIF-mediated mechanism.MethodsJurkat cells were cultured in Roswell Park Memorial Institute media, at a final concentration of 2.5 × 106 cell/mL. The effects of HTS on T-cell proliferation following PGE2-induced suppression were evaluated in Jurkat cells: HTS at 20 or 40 mmol/L above isotonicity was added. MIF levels were determined by enzyme-linked immunosorbent assay and western blot analysis.ResultsPGE2 caused a 15.0% inhibition of Jurkat cell proliferation, as compared to the control. MIF levels decreased in PGE2-suppressed cells, as compared to the control. MIF levels were higher in cells treated with HTS than PGE2-stimulated cells.ConclusionThe role of HTS in restoring Jurkat cells proliferation suppressed by PGE2, at least in part, should be mediated through a MIF pathway.

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Intracellular detection of macrophage migration inhibitory factor in peripheral blood leukocytes

Cited by 14 publications

References 51 publications

Regulation of IL-1 and TNF Receptor Expression and Function by Endogenous Macrophage Migration Inhibitory Factor

Regulation of IL-1 and TNF Receptor Expression and Function by Endogenous Macrophage Migration Inhibitory Factor

Human Plasma Membrane-Derived Vesicles Halt Proliferation and Induce Differentiation of THP-1 Acute Monocytic Leukemia Cells

Effect of hypertonic saline and macrophage migration inhibitory factor in restoration of T cell dysfunction

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