IL-4 Decreases the Expression of the Monocyte Differentiation Marker CD14, Paralleled by an Increasing Accessory Potency
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2023, Biochemical and Biophysical Research CommunicationsCD14<sup>++</sup> CD16<sup>−</sup> monocytes are the main source of 11β-HSD type 1 after IL-4 stimulation
2017, International ImmunopharmacologyCitation Excerpt :When used in combination with the glucocorticoid dexamethasone, F8-IL4 was able to cure mice with established collagen-induced arthritis fully human version of F8-IL4 is currently being developed for clinical investigations [41]. IL-4 is a pleiotropic cytokine produced by activated T cells that has been discussed as a monocyte activating protein that affects the phenotype and functions of human monocytes and macrophages [42]. It has already been demonstrated that blood monocytes stimulated with IL-4 showed an increase in 11β-HSD1 activity [3], but it is still unknown if all monocyte subsets respond to IL-4 induction in a similar way or if the increased 11β-HSD1 activity after exposure to IL-4 is specific to one of the monocyte subpopulations.
Differential modulation of CCR5-tropic human immunodeficiency virus-1 transfer from macrophages towards T cells under interleukin-4/interleukin-13 microenvironment
2010, Human ImmunologyCitation Excerpt :All MDM populations were adherent cells (not shown). As expected, M-4 and M-13 did not acquire dendritic cell markers CD1a and CD83 [19], and did not express CD14 and CD16, consistent with previous studies [20–22] (Fig. 1A). All MDM populations expressed CD40, CD80, HLA-DR, CD44, CD11a, CD11b, and CD11c at similar level.
Low-affinity IgE receptor (FcεRII)-mediated activation of human monocytes by both monomeric IgE and IgE/anti-IgE immune complex
2009, International ImmunopharmacologyRetinoic acid inhibits dendritic cell differentiation driven by interleukin-4
2009, Cellular ImmunologyCitation Excerpt :The role of IL-4 on DC generation from peripheral blood monocytes (PBMC) is not only to suppress the monocyte and/or macrophage lineage but it actively promotes the differentiation of monocytes along the DC lineage [24,25]. IL-4 alone is showed to be capable of up-regulate MHC class-II molecules, co-stimulatory molecules and down-regulate CD14 on monocytes [26–28]. More recently it was demonstrated that IL-4, without the involvement of endogenous or exogenous GM-CSF, transforms human peripheral blood monocytes to a CD1a diminished myeloid DC subset [29].
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Dr. J.H Peters, Abteilung Immunologie, Kreuzbergring 57, 3400 Güttingen, Germany