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Induction of macrophage inflammatory protein-1 beta gene expression in human monocytes by lipopolysaccharide and IL-7
S F Ziegler1, T W Tough, T L Franklin
1Department of Molecular Biology, Immunex Corporation, Seattle, WA 98101.
Abstract:
HuMIP-1 beta is a member of a gene family of inflammatory cytokines whose expression is induced by proinflammatory and mitogenic stimuli. The gene was rapidly induced in human peripheral blood monocytes by either LPS or IL-7. However, IL-7 was unable to induce HuMIP-1 beta mRNA in peripheral blood T cells. The induction of HuMIP-1 beta mRNA in monocytes by IL-7 or LPS was inhibited by IL-4. The 5'-regulatory region of the HuMIP-1 beta gene was cloned and sequenced. An analysis of this sequence revealed three consensus-binding sites for the nuclear factor PU.1 and three potential glucocorticoid response elements. However, the HuMIP-1 beta gene appears to be unresponsive to dexamethasone. Also present in the 5'-regulatory region was a LPS-responsive element located within 455 bp 5' to the start of transcription.
Insights
Human inflammatory cytokine HuMIP-1 beta (Human Migration Inhibitory Protein-1 beta) gene expression is induced by LPS and IL-7 in monocytes but not T cells. IL-4 inhibits this induction, and regulatory elements were identified in the gene’s 5’ region.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- HuMIP-1 beta (Human Migration Inhibitory Protein-1 beta) is an inflammatory cytokine involved in immune responses.
- Cytokine gene expression is regulated by various stimuli and cellular contexts.
- Understanding the regulation of HuMIP-1 beta is crucial for comprehending inflammatory processes.
Purpose of the Study:
- To investigate the induction of HuMIP-1 beta gene expression in human peripheral blood monocytes and T cells.
- To identify regulatory elements within the 5'-regulatory region of the HuMIP-1 beta gene.
- To explore the effects of specific stimuli (LPS, IL-7) and inhibitors (IL-4, dexamethasone) on HuMIP-1 beta expression.
Main Methods:
- Cloning and sequencing of the 5'-regulatory region of the HuMIP-1 beta gene.
- Analysis of the 5'-regulatory sequence for potential transcription factor binding sites and response elements.
- Experimental induction of HuMIP-1 beta mRNA in human peripheral blood monocytes and T cells using LPS and IL-7, with subsequent assessment of IL-4 and dexamethasone effects.
Main Results:
- HuMIP-1 beta gene expression was rapidly induced in monocytes by lipopolysaccharide (LPS) and IL-7, but not in T cells.
- Interleukin-4 (IL-4) inhibited the induction of HuMIP-1 beta mRNA in monocytes by both IL-7 and LPS.
- The 5'-regulatory region contains PU.1 binding sites, potential glucocorticoid response elements, and an LPS-responsive element within 455 bp upstream of transcription start.
Conclusions:
- HuMIP-1 beta expression is differentially regulated in monocytes and T cells, with monocytes showing rapid induction by inflammatory stimuli.
- IL-4 acts as an inhibitor of HuMIP-1 beta induction in monocytes, suggesting a role in modulating inflammatory responses.
- The identified regulatory elements in the 5'-region, including PU.1 sites and an LPS-responsive element, are key to understanding HuMIP-1 beta gene control.
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