ArticleJournal of clinical immunology1994
Differential induction of human monocyte transforming growth factor beta 1 production and its regulation by interleukin 4.
Article in Journal of clinical immunology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 17 citations in OpenAlex.
- TGF-β/IFN-γ Antagonism in Subversion and Self-Defense of Phase II Coxiella burnetiiInfection and immunity · 2023Trial
- Norepinephrine modulates myelopoiesis after experimental thermal injury with sepsis.Annals of surgery · 2001Article
- Production of interleukin-10 and transforming growth factor beta by peripheral blood mononuclear cells in Q fever endocarditis.Infection and immunity · 1996Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously shown that trauma patients' monocytes which are in vivo activated by multiple injury-induced mediators have elevated transforming growth factor-beta (TGF beta) bioactivity. Interleukin-4 (IL-4), a Th2 and B lymphocyte stimulatory factor, has been shown to inhibit monocyte production of a number of mediators both after lipopolysaccharide stimulation and after trauma-induced stimulation. However, IL-4 inhibitory effects appears to vary, depending on the mixture of inducing stimuli. Here we describe the in vitro IL-4 inhibition of human monocyte TGF beta bioactivity using several stimulation induction protocols: muramyl dipeptide stimulation alone, or after Fc gamma RI (CD64) cross-linking induction, interferon-gamma (IFN gamma) priming, or trauma-generated in vivo mediator induction. IL-4 suppressed both muramyl dipeptide-induced TGF beta bioactivity and TGF beta mRNA in a dose-dependent fashion and was most effective when IL-4 was administered at initiation of normal monocyte stimulation. Muramyl dipeptide (MDP)-induced increases in trauma patients' monocyte TGF beta bioactivity were also inhibited by high doses of IL-4 (25 ng/ml). Fc gamma RI cross-linking increased MDP-induced normal monocyte TGF beta bioactivity, but this increase could be consistently inhibited only by very high IL-4 concentrations (50 ng/ml). IL-4 did not consistently downregulate MDP-induced TGF beta bioactivity in IFN gamma-primed monocytes. IL-4 can suppress monocyte TGF beta production, as well as other monocyte mediators, but its efficiency depends on the stimuli combination present in the microenvironment.
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