Monocyte Dependent Regulation of Autoimmune Inflammation

Nicholson, Lindsay B.; Raveney, Ben J. E.; Munder, Markus

doi:10.2174/156652409787314499

Cited by 55 publications

(42 citation statements)

References 63 publications

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“…In addition, Mu-like cells, called MDSC, 16 isolated under other chronic inflammatory situations, particularly from tumours, and that suppress anti-tumour immune responses, have been described previously. [17][18][19] These cells exhibit a range of characteristics that are unlikely to be controlled directly by TNFR1 signalling.…”

Section: Discussionmentioning

confidence: 99%

TNFR1 signalling is a critical checkpoint for developing macrophages that control of T‐cell proliferation

et al. 2010

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SummaryMacrophages (Mu) are professional antigen-presenting cells, but when they accumulate at sites of inflammation, they can inhibit T-cell proliferation. In experimental autoimmune uveoretinitis, this limits the expansion of T cells within the target organ. To define requirements for the elaboration of this outcome, we have generated populations of Mu in vitro that could also regulate T-cell responses; stimulating CD4 + T-cell activation and cytokine production, but simultaneously suppressing T-cell proliferation. When T cells are removed from the influence of such cells, normal T-cell responses are restored. We show that tumour necrosis factor 1 (TNFR1) signalling is a critical checkpoint in the development of such Mu, as TNFR1 )/) Mu are unable to suppress T-cell proliferation. This deficit in antigen-presenting cells results in a lack of production of prostaglandin E 2 (PGE 2 ) and nitric oxide, which are critical effector mechanisms that inhibit T-cell division. However, TNFR1 signalling is not required for the inhibitory function of Mu because we could circumvent the requirement for this receptor, by maturing Mu in the presence of exogenous interferon-c and PGE 2 . This produced TNFR1 )/) Mu that inhibited T-cell proliferation and indicates that TNFR1 delivers a signal that is necessary for the development but not the execution of this function.

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Section: Discussionmentioning

confidence: 99%

TNFR1 signalling is a critical checkpoint for developing macrophages that control of T‐cell proliferation

et al. 2010

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“…Effector T cells commonly exert their functions in tissues subjected to oxidative stress (10,11), but the mechanisms explaining how Ag-specific T cells survive in these hostile environments remain incompletely understood. This study showed that DCs furnish effector T cells with cs-and ic-thiols during presentation of viral and bacterial Ags and that T cells with enhanced thiol expression consume ROS and escape oxidant-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…After Ag presentation in lymphoid tissue, Ag-specific T cells home to the site of infection where they combat infection in a potentially hostile oxidative microenvironment (10,11). To clarify the functional consequences of DC-induced thiol expression by T cells, we tested whether DC-stimulated T cells had acquired the capacity to neutralize oxygen radicals.…”

Section: T Cells Activated By Dcs Neutralize H 2 O 2 and Escape Oxidamentioning

confidence: 99%

“…For example, T cells and other lymphocytes rapidly become inactivated and eventually undergo apoptosis when exposed to ROS (6)(7)(8)(9). Because effector T cells commonly exert their functions in the oxidative environment characteristic of infected or inflamed tissues (10,11), it is conceivable that T cells use strategies to escape oxygen radical-induced inactivation.…”

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confidence: 99%

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Redox Remodeling by Dendritic Cells Protects Antigen-Specific T Cells against Oxidative Stress

Martner

Aurelius

Rydström

et al. 2011

The Journal of Immunology

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Microorganisms and microbial products induce the release of reactive oxygen species (ROS) from monocytes and other myeloid cells, which may trigger dysfunction and apoptosis of adjacent lymphocytes. Therefore, T cell-mediated immunity is likely to comprise mechanisms of T cell protection against ROS-inflicted toxicity. The present study aimed to clarify the dynamics of reduced sulfhydryl groups (thiols) in human T cells after presentation of viral and bacterial Ags by dendritic cells (DCs) or B cells. DCs, but not B cells, efficiently triggered intra- and extracellular thiol expression in T cells with corresponding Ag specificity. After interaction with DCs, the Ag-specific T cells acquired the capacity to neutralize exogenous oxygen radicals and resisted ROS-induced apoptosis. Our results imply that DCs provide Ag-specific T cells with antioxidative thiols during Ag presentation, which suggests a novel aspect of DC/T cell cross-talk of relevance to the maintenance of specific immunity in inflamed or infected tissue.

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“…Myeloid-derived suppressor cells (MDSCs) represent a heterogeneous population of cells that accumulate during autoimmunity and other pathological conditions (1). The activation of MDSCs in pathological conditions leads to the upregulation of the expression of immune suppressive factors, resulting in MDSC-mediated suppression of T cell functions (2).…”

Section: Introductionmentioning

confidence: 99%

Myeloid-derived suppressor cells and myeloid regulatory cells in cancer and autoimmune disorders

Barnie

Zhang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Myeloid-derived suppressor cells (MDSCs) were originally described as a heterogeneous population of immature cells derived from myeloid progenitors with immune-suppressive functions in tumor-bearing hosts. In recent years, increasing number of studies have described various populations of myeloid cells with MDSC-like properties in murine models of cancer and autoimmune diseases. These studies have observed that the populations of MDSCs are increased during inflammation and autoimmune conditions. In addition, MDSCs can effectively suppress T cell responses and modulate the activity of natural killer cells and other myeloid cells. MDSCs have also been implicated in the induction of regulatory T cell production. Furthermore, these cells have the potential to suppress the autoimmune response, thereby limiting tissue injury. Myeloid regulatory cells (Mregs) are recently attracting increasing attention, since they function in proinflammatory and immune suppression in autoimmune diseases, as well as in various types of cancer. Currently, research focus is directed from MDSCs to Mregs in cancer and autoimmune diseases. The present study reviewed the suppressive roles of MDSCs in various autoimmune murine models, the immune modulation of MDSCs to T helper 17 lymphocytes, as well as the proinflammatory and immunosuppressive roles of Mregs in various types of cancer and autoimmune diseases.

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Monocyte Dependent Regulation of Autoimmune Inflammation

Cited by 55 publications

References 63 publications

TNFR1 signalling is a critical checkpoint for developing macrophages that control of T‐cell proliferation

TNFR1 signalling is a critical checkpoint for developing macrophages that control of T‐cell proliferation

Redox Remodeling by Dendritic Cells Protects Antigen-Specific T Cells against Oxidative Stress

Myeloid-derived suppressor cells and myeloid regulatory cells in cancer and autoimmune disorders

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