Selective expansion of CD16highCCR2– subpopulation of circulating monocytes with preferential production of haem oxygenase (HO)-1 in response to acute inflammation

Mizuno, Kazunori; Toma, Tomoko; Tsukiji, Hidenori; Okamoto, Hiroyuki; Yamazaki, Haruyuki; Ohta, Kunio; Kasahara, Yoshihito; Koizumi, Satoshi; Yachie, Akihiro

doi:10.1111/j.1365-2249.2005.02932.x

Cited by 66 publications

(53 citation statements)

References 41 publications

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“…The present concept is that these monocyte subsets represent distinct developmental stages, with the intermediate subset being the direct intermediary link between the immature classical and the more mature nonclassical monocyte subsets (2), and that M-CSF contributes to this differentiation (4,5). Functional studies have shown that CD16 + monocytes are the main source of TNF and IL-1b upon TLR-2, -4, -7, or -8 stimulation (6)(7)(8). Moreover, their blood numbers significantly increase in chronic inflammatory conditions (9).…”

Section: Cd16mentioning

confidence: 99%

Atypical Activin A and IL-10 Production Impairs Human CD16+ Monocyte Differentiation into Anti-Inflammatory Macrophages

González-Domínguez

Domínguez-Soto

Nieto

et al. 2016

The Journal of Immunology

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Human CD14++CD16− and CD14+/loCD16+ monocyte subsets comprise 85 and 15% of blood monocytes, respectively, and are thought to represent distinct stages in the monocyte differentiation pathway. However, the differentiation fates of both monocyte subsets along the macrophage (Mϕ) lineage have not yet been elucidated. We have now evaluated the potential of CD14++ CD16− and CD16+ monocytes to differentiate and to be primed toward pro- or anti-inflammatory Mϕs upon culture with GM-CSF or M-CSF, respectively (subsequently referred to as GM14, M14, GM16, or M16). Whereas GM16 and GM14 were phenotypic and functionally analogous, M16 displayed a more proinflammatory profile than did M14. Transcriptomic analyses evidenced that genes associated with M-CSF–driven Mϕ differentiation (including FOLR2, IL10, IGF1, and SERPINB2) are underrepresented in M16 with respect to M14. The preferential proinflammatory skewing of M16 relative to M14 was found to be mediated by the secretion of activin A and the low levels of IL-10 produced by M16. In fact, activin A receptor blockade during the M-CSF–driven differentiation of CD16+ monocytes, or addition of IL-10–containing M14-conditioned medium, significantly enhanced their expression of anti-inflammatory–associated molecules while impairing their acquisition of proinflammatory-related markers. Thus, we propose that M-CSF drives CD14++CD16ˉ monocyte differentiation into bona fide anti-inflammatory Mϕs in a self-autonomous manner, whereas M-CSF–treated CD16+ monocytes generate Mϕs with a skewed proinflammatory profile by virtue of their high activin A expression unless additional anti-inflammatory stimuli such as IL-10 are provided.

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Section: Cd16mentioning

confidence: 99%

Atypical Activin A and IL-10 Production Impairs Human CD16+ Monocyte Differentiation into Anti-Inflammatory Macrophages

González-Domínguez

Domínguez-Soto

Nieto

et al. 2016

The Journal of Immunology

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“…A group of 11 healthy individuals (age [18][19][20][21][22][23][24][25][26][27][28][29][30] were studied before and after physical exercise on a home-trainer bike at 200 watts (W) either for 1 min or to exhaustion for 3-10 min. In addition, we analyzed four patients with inflammatory diseases.…”

Section: Subjectsmentioning

confidence: 99%

Standardized single‐platform assay for human monocyte subpopulations: Lower CD14⁺CD16⁺⁺ monocytes in females

et al. 2010

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We present a novel single-platform assay for determination of the absolute number of human blood monocyte subpopulations, i.e., the CD14 11 CD16 2 and the CD14 1 CD16 11 monocytes. A four-color combination of antibodies to CD14, CD16, CD45, and HLA-DR reduces the spill-over of natural killer cells and of granulocytes into the CD14 1 CD16 11 monocyte gate. For these CD14 1 CD16 11 monocytes, the intra-assay coefficient of variation (CV) was 4.1% and the inter-assay CV was 8.5%. Looking at a cohort of 40 donors aged 18-60 years, we found no age dependence. There was however an effect of gender in that females had lower CD14 1 CD16 11 monocytes (45.4 AE 13.5 cells/ll) compared with males (59.1 AE 20.3 cells/ll) (P < 0.02). Using this novel approach, we can confirm that exercise will lead to more than three-fold increase of the CD14 1 CD16 11 monocytes. Also, we show that therapy with low doses of glucocorticoids will deplete these cells. This robust single-platform assay may be a useful tool for monitoring the absolute number of monocyte subpopulations in health and disease. ' International Society for Advancement of CytometryKey terms monocyte heterogeneity; gender; exercise; glucocorticoids MYELOMONOCYTIC stem cells in bone marrow give rise to monocytes and these are released into blood where they circulate for a few days and then migrate into tissue where they develop into different types of macrophages (1). Monocytes were initially defined based on morphology and cytochemistry. With the advent of monoclonal antibodies and flow cytometry, human monocytes were characterized with antibodies like CD14. This technology also allowed for the definition of two monocyte subsets, i.e., the classical CD14 11 CD162 and the CD14 1 CD16 11 nonclassical monocytes (2) with the latter cells characterized by higher MHC class II expression and by higher production of the cytokine tumor necrosis factor (3). With the recognition of the potential role of the nonclassical CD14

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“…2013. 43: 335-347 an imbalance in the relative proportions of the subsets during acute inflammation [5] and several infectious diseases [6][7][8][9][10] including tuberculosis (TB) [11,12] has been described. TB, a disease that mainly affects the respiratory system, infects onethird of the world's population and kills 2 million people each year [13].…”

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confidence: 99%

Impaired dendritic cell differentiation of CD16‐positive monocytes in tuberculosis: Role of p38 MAPK

et al. 2013

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Tuberculosis (TB) is one of the world's most pernicious diseases mainly due to immune evasion strategies displayed by its causative agent Mycobacterium tuberculosis (Mtb). Blood monocytes (Mos) represent an important source of DCs during chronic infections; consequently, the alteration of their differentiation constitutes an escape mechanism leading to mycobacterial persistence. We evaluated whether the CD16 + /CD16 − Mo ratio could be associated with the impaired Mo differentiation into DCs found in TB patients. The phenotype and ability to stimulate Mtb-specific memory clones DCs from isolated Mo subsets were assessed. We found that CD16 − Mos differentiated into CD1a + DC-SIGN high cells achieving an efficient recall response, while CD16 + Mos differentiated into a CD1a − DC-SIGN low population characterized by a poor mycobacterial Ag-presenting capacity. The high and sustained phosphorylated p38 expression observed in CD16 + Mos was involved in the altered DC profile given that its blockage restored DC phenotype and its activation impaired CD16 − Mo differentiation. Furthermore, depletion of CD16 + Mos indeed improved the differentiation of Mos from TB patients toward CD1a + DC-SIGN high DCs. Therefore, Mos from TB patients are less prone to differentiate into DCs due to their increased proportion of CD16 + Mos, suggesting that during Mtb infection Mo subsets may have different fates after entering the lungs. Keywords: Dendritic cells r Monocyte differentiation r Tuberculosis See accompanying Commentary by Lugo-Villarino and NeyrollesAdditional supporting information may be found in the online version of this article at the publisher's web-site IntroductionMonocytes (Mos) are large circulating leukocytes of the myeloid lineage that mediate essential functions of innate immunity including phagocytosis and cytokine production [1,2]. Mos are produced Correspondence: Dr. Luciana Balboa e-mail: luciana_balboa@hotmail.com in the bone marrow and released into the blood, and circulate in blood or reside in a spleen reservoir and, upon tissue infiltration they can differentiate into macrophages (M s) or DCs. Although human blood Mos are a highly heterogeneous population, two main subsets have been described: CD14 + CD16 − "classical" Mos are the major Mo population and CD14 + CD16 + Mos, the minor one (5-10% of total Mos). The latter subset has a more mature phenotype and an enhanced proinflammatory activity [3]. This heterogeneity has led to the hypothesis that Mos are committed to specific functions prior to tissue infiltration [4]. Also, C 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu 336Luciana Balboa et al. Eur. J. Immunol. 2013. 43: 335-347 an imbalance in the relative proportions of the subsets during acute inflammation [5] and several infectious diseases [6][7][8][9][10] including tuberculosis (TB) [11,12] has been described. TB, a disease that mainly affects the respiratory system, infects onethird of the world's population and kills 2 million people each year [13]. The success o...

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Selective expansion of CD16highCCR2– subpopulation of circulating monocytes with preferential production of haem oxygenase (HO)-1 in response to acute inflammation

Cited by 66 publications

References 41 publications

Atypical Activin A and IL-10 Production Impairs Human CD16+ Monocyte Differentiation into Anti-Inflammatory Macrophages

Atypical Activin A and IL-10 Production Impairs Human CD16+ Monocyte Differentiation into Anti-Inflammatory Macrophages

Standardized single‐platform assay for human monocyte subpopulations: Lower CD14⁺CD16⁺⁺ monocytes in females

Impaired dendritic cell differentiation of CD16‐positive monocytes in tuberculosis: Role of p38 MAPK

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Selective expansion of CD16highCCR2– subpopulation of circulating monocytes with preferential production of haem oxygenase (HO)-1 in response to acute inflammation

Cited by 66 publications

References 41 publications

Atypical Activin A and IL-10 Production Impairs Human CD16+ Monocyte Differentiation into Anti-Inflammatory Macrophages

Atypical Activin A and IL-10 Production Impairs Human CD16+ Monocyte Differentiation into Anti-Inflammatory Macrophages

Standardized single‐platform assay for human monocyte subpopulations: Lower CD14+CD16++ monocytes in females

Impaired dendritic cell differentiation of CD16‐positive monocytes in tuberculosis: Role of p38 MAPK

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Standardized single‐platform assay for human monocyte subpopulations: Lower CD14⁺CD16⁺⁺ monocytes in females