Interleukin-10 in combination with M-CSF and IL-4 contributes to development of the rare population of CD14+CD16++ cells derived from human monocytes

Li, Geling; Hangoc, Giao; Broxmeyer, Hal E.

doi:10.1016/j.bbrc.2004.07.172

Cited by 16 publications

(12 citation statements)

References 26 publications

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“…Because they are different from typical macrophages as well as DCs, we have termed this type of accessory cell M-DC in contrast to GM-CSF/IL-4-induced DCs and M-CSF-induced macrophages. Consistent with our previous report (61), no osteoclast-like multinucleated giant cells appeared in 1 wk of culture with M-CSF and IL-4. M-CSF/IL-4 has been reported to induce the generation of a large amount of multinucleated giant cells in 2 wk of cell culture (51).…”

Section: Discussionsupporting

confidence: 93%

Macrophage Colony-Stimulating Factor Drives Cord Blood Monocyte Differentiation into IL-10highIL-12absent Dendritic Cells with Tolerogenic Potential

Kim

Broxmeyer

2005

The Journal of Immunology

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Immature dendritic cells (DCs) induce tolerance and mature DCs induce inflammatory immune responses. However, the likelihood of maturation of immature DCs in vivo limits its potential application for suppression of unwanted immune reactions in vivo. The aim of this study was to generate DCs with anti-inflammatory properties in both the immature and mature states. GM-CSF combined with IL-4 drives monocyte differentiation into DCs. As M-CSF is a critical cytokine in development of the monocytic lineage and its level is dramatically elevated in immunosuppressive conditions, we investigated whether M-CSF could replace GM-CSF and generate DCs with distinct functions from umbilical cord blood monocytes. Highly purified umbilical cord blood monocytes cultured with M-CSF and IL-4, in a GM-CSF-independent fashion, differentiated into IL-10highIL-12absent cells with a DC phenotype (termed M-DC). Single time stimulation with immature DCs (both M-DCs and DCs) derived from cord blood induced hyporesponsive and regulatory CD4+ T cells. In contrast to mature DCs, mature M-DCs induced decreased Th1 differentiation and proliferation of naive CD4+ T cells in both primary and secondary allogeneic MLR and showed tolerogenic potential. These results demonstrate an unrecognized role for M-CSF in alternative differentiation of monocytes into anti-inflammatory M-DCs and suggest that M-CSF-induced DCs may be of use for suppressing unwanted immune responses.

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Section: Discussionsupporting

confidence: 93%

Macrophage Colony-Stimulating Factor Drives Cord Blood Monocyte Differentiation into IL-10highIL-12absent Dendritic Cells with Tolerogenic Potential

Kim

Broxmeyer

2005

The Journal of Immunology

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“…DC-SIGN is a type II transmembrane C-type lectin with a carbohydrate recognition domain, which is expressed in human DCs and macrophages (Geijtenbeek et al, 2000; Soilleux et al, 2002), and is involved in multiple aspects of the immunological response (van Kooyk and Geijtenbeek, 2003). Broxmeyer and colleagues reported that in vitro differentiation of monocytes in the presence of M-CSF and IL-4, which induces DC-SIGN expression (Martinez et al, 2006), are less efficient inductors of allogeneic mixed lymphocyte reactions (Li et al, 2004; Li et al, 2005). Here, we extend these findings to newly demonstrate that DC-SIGN + macrophages inhibit T cell proliferation in vitro and in vivo in an experimental mouse model of solid organ transplantation.…”

Section: Discussionmentioning

confidence: 99%

DC-SIGN+ Macrophages Control the Induction of Transplantation Tolerance

et al. 2015

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SUMMARY Tissue effector cells of the monocyte lineage can differentiate into different cell types with specific cell function depending on their environment. The phenotype, developmental requirements, and functional mechanisms of immune protective macrophages that mediate the induction of transplantation tolerance remain elusive. Here, we demonstrate that costimulatory blockade favored accumulation of DC-SIGN-expressing macrophages that inhibited CD8+ T cell immunity and promoted CD4+Foxp3+ Treg cell expansion in numbers. Mechanistically, that simultaneous DC-SIGN engagement by fucosylated ligands and TLR4 signaling was required for production of immunoregulatory IL-10 associated with prolonged allograft survival. Deletion of DC-SIGN-expressing macrophages in vivo, interfering with their CSF1-dependent development, or preventing the DC-SIGN signaling pathway abrogated tolerance. Together, the results provide new insights into the tolerogenic effects of costimulatory blockade and identify DC-SIGN+ suppressive macrophages as crucial mediators of immunological tolerance with the concomitant therapeutic implications in the clinic.

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“…Interestingly, as mentioned earlier, an increase in the number of circulating CD14 + monocytes that co-express CD16 has been seen in patients with HIV-1 dementia (Pulliam et al, 1997; Fischer-Smith et al, 2001), and in vitro studies show CD16 upregulation by monocytes when treated with M-CSF (Ji et al, 2000; Saionji and Ohsaka, 2001). In combination with IL-10 and IL-4, M-CSF also contributes to the development of CD14+CD16+ monocytes that produce high levels of TNF-α and IL-1β (Li et al, 2004). CD163 is also up-regulated by M-CSF treatment of human monocytes (Buechler et al, 2000).…”

Section: Neurotoxic Products Released By Infected Macrophagesmentioning

confidence: 99%

CNS Inflammation and Macrophage/Microglial Biology Associated with HIV-1 Infection

Yadav

Collman

2009

J Neuroimmune Pharmacol

172

145

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HIV-1 infection of the central nervous system (CNS) can result in neurological dysfunction with devastating consequences in a significant proportion of individuals with AIDS. HIV-1 does not infect neurons directly, but induces damage indirectly through the accumulation of activated macrophage/microglia (M/M) cells, some of which are infected, that release neurotoxic mediators including both cellular activation products and viral proteins. One mechanism for the accumulation of activated M/M involves the development in infected individuals of an activated peripheral blood monocyte population that traffics through the blood brain barrier (BBB), a process that also serves to carry virus into CNS and establish local infection. A second mechanism involves the release by infected and activated M/M in the CNS of chemotactic mediators that recruit additional monocytes from the periphery. These activated M/M, some of which are infected, release a number of cytokines and small molecule mediators as well as viral proteins that act on bystander cells and in turn activate them, thus amplifying the cascade. These viral proteins and cellular products have neurotoxic properties as well, both directly and through induction of astrocyte dysfunction, which ultimately lead to neuronal injury and death. In patients effectively treated with antiretroviral therapy, frank dementia is now uncommon and has been replaced by milder forms of neurocognitive impairment, with less frequent and more focal neuropathology. This review summarizes key findings that support the critical role and mechanisms of monocyte/macrophage activation and inflammation as a major component for HIV-1 encephalitis or HIV-1 associated dementia.

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Interleukin-10 in combination with M-CSF and IL-4 contributes to development of the rare population of CD14+CD16++ cells derived from human monocytes

Cited by 16 publications

References 26 publications

Macrophage Colony-Stimulating Factor Drives Cord Blood Monocyte Differentiation into IL-10highIL-12absent Dendritic Cells with Tolerogenic Potential

Macrophage Colony-Stimulating Factor Drives Cord Blood Monocyte Differentiation into IL-10highIL-12absent Dendritic Cells with Tolerogenic Potential

DC-SIGN+ Macrophages Control the Induction of Transplantation Tolerance

CNS Inflammation and Macrophage/Microglial Biology Associated with HIV-1 Infection

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