Macrophage Migration Inhibitory Factor (MIF) Produced by a Human T Cell Hybridoma Clone

Hirose, S; Ooki, Shinji; Higuchi, Masahiro; Osawa, Toshiaki

doi:10.1111/j.1348-0421.1991.tb01552.x

Cited by 5 publications

(2 citation statements)

References 17 publications

(10 reference statements)

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“…It is now known to be widely expressed in various cell types, including activated T cells, macrophages and anterior pituitary gland cells, etc. [ 7 – 10 ]. In addition to macrophage migration inhibition, other functions of MIF have yet to be fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Macrophage migration inhibitory factor enhances lipopolysaccharide-induced fibroblast proliferation by inducing toll-like receptor 4

Xie

Yang

2016

BMC Musculoskelet Disord

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BackgroundFibroblast proliferation is a common manifestation of chronic inflammatory diseases, including rheumatoid arthritis (RA), Crohn’s disease and ulcerative colitis, etc. To alleviate patient suffering, the mechanism underlying fibroblast proliferation should be elucidated.MethodsCCK-8 assay was used to assess the stimulatory effect of LPS and macrophage migration inhibitory factor (MIF) on fibroblast proliferation. Then, TLR4 expression on fibroblast cell membrane was carried out by confocal scanning microscopy. Finally, real-time fluorescent quantitative PCR and flow cytometry were applied to determine the expression of TLR4 after MIF challenge.ResultsLPS alone directly stimulated the fibroblast proliferation. In addition, MIF showed co-stimulatory effect on LPS-induced fibroblast proliferation. Interestingly, fibroblast overtly expressed TLR4 without stimulation. After MIF stimulation, real-time PCR showed TLR4 mRNA levels were increased by about 33 % in the fibroblasts; in agreement, TLR4 expression on the fibroblast membrane was increased by about 20 %, as shown by flow cytometry.ConclusionsThese findings indicated MIF elevates TLR4 expression in fibroblast, enhancing LPS-induced cell proliferation.

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Section: Discussionmentioning

confidence: 99%

Macrophage migration inhibitory factor enhances lipopolysaccharide-induced fibroblast proliferation by inducing toll-like receptor 4

Xie

Yang

2016

BMC Musculoskelet Disord

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“…(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) This cell selection method was used to omit HAT cytotoxicity. The F3B6 heteromyeloma cells were cultured at 10 6 streptomycin, 0.1 mM hypoxanthine, 0.016 mM thymidine (all from Sigma, St. Louis, MO), and 10% fetal bovine serum (FBS, Gibco, BRL Life Technologies) (complete RPMI medium) in the presence of 5Â10 À5 M emetine-Cl and 0.25 mg=mL actinomycin D (both from Sigma) for 2 h in a humidified 378C, 5% CO 2 incubator prior to fusion.…”

Section: Pretreatment Of F3b6 Cells With Actinomycin D and Emetinementioning

confidence: 99%

An Extreme Strategy for the Production of Hybridoma

2009

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The ethical issues surrounding human immunization hamper the production of human monoclonal antibody through scarcity of immunized B cells in peripheral blood. This defect can be compensated in part by improvement of hybridoma production techniques. We have developed a new strategy to bypass the toxic effects of polyethylene glycol (PEG) as fusogenic reagent and hypoxanthine aminoptrin thymidine (HAT) as selective medium on newly fused cells. The Epstein-Barr virus (EBV) transformed peripheral blood mononuclear cells (PBMC) of accidentally Rh antigen sensitized persons were fused using cephalin as fugenic reagent, with emetine and actinomycin D pretreated heteromyeloma cells. Our results showed that 19-34% of EBV-transformed B cells were grown as hybridoma clones following selection. This extreme improvement in hybridoma production rate may end the fusion efficiency problem and make hybridoma production a plug-and-play technology.

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Rat liver protein linking chemical and immunological detoxification systems

Blocki

Schlievert

Wackett

1992

Nature

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Mammals have separate enzymatic and cellularly mediated detoxification systems. Glutathione S-transferases (GSTs) protect against xenobiotic chemicals which continuously enter the body, largely through mucous membranes. These enzymes catalyse the conjugation of glutathione with a wide variety of electrophilic compounds rendering them non-toxic. Mammals also mount a cellular immunological response on entry of foreign cells, viruses or macromolecules into the body. T lymphocytes mobilize at the site of foreign body entry and secrete protein messengers called lymphokines. Secondary to T lymphocytes, macrophages concentrate at the infection site and function in antigen processing and phagocytosis. In vitro, macrophage movement is arrested by one class of lymphokines known as macrophage migration inhibitory factors (MIFs). We report here the purification of milligram quantities of a unique multifunctional protein from rat liver which links enzymatic and immunological detoxification systems. This protein actuates both GST and MIF activity and matches the primary structure of a human MIF in 25 out of 26 amino-terminal amino acids. Primary structure comparisons revealed significant similarity between GSTs and MIF. The glutathione affinity chromatography purification described here yields a 100-fold increase in obtaining MIF and will aid understanding of its precise biological function.

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Macrophage Migration Inhibitory Factor (MIF) Produced by a Human T Cell Hybridoma Clone

Cited by 5 publications

References 17 publications

Macrophage migration inhibitory factor enhances lipopolysaccharide-induced fibroblast proliferation by inducing toll-like receptor 4

Macrophage migration inhibitory factor enhances lipopolysaccharide-induced fibroblast proliferation by inducing toll-like receptor 4

An Extreme Strategy for the Production of Hybridoma

Rat liver protein linking chemical and immunological detoxification systems

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