Loss of Myeloid Related Protein-8/14 Exacerbates Cardiac Allograft Rejection

Shimizu, Koïchi; Libby, Peter; Rocha, Viviane Z.; Folco, Eduardo J.; Shubiki, Rica; Grabie, Nir; Jang, Sunyoung; Lichtman, Andrew H.; Shimizu, Ayako; Hogg, Nancy; Simon, Daniel I.; Mitchell, Richard N.; Croce, Kevin

doi:10.1161/circulationaha.110.009910

Cited by 31 publications

(20 citation statements)

References 59 publications

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“…The expansion of MDSC was significantly reduced in S100A9-deficient tumor-bearing mice and mice treated with complete Freund's adjuvant (CFA) (21, 22). Consistent with these findings, DCs derived from S100A9-deficient mice induced stronger response of allogeneic T cells (23). …”

Section: Introductionsupporting

confidence: 58%

Myeloid-Derived Suppressor Cells in the Development of Lung Cancer

Ortiz

Lu²,

Ramachandran

et al. 2014

Cancer Immunology Research

100

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Myeloid-derived suppressor cells (MDSC) are widely implicated in immune suppression associated with tumor progression and chronic inflammation. However, very little is known about their possible role in tumor development. Here, we evaluated the role of MDSC in two experimental models of lung cancer: inflammation-associated lung cancer caused by chemical carcinogen urethane in combination with exposure to cigarette smoke (CS); and transgenic CC10Tg model not associated with inflammation. Exposure of mice to CS alone resulted in significant accumulation in various organs of cells with typical MDSC phenotype (Gr-1+CD11b+). However, these cells lacked immune suppressive activity and could not be defined as MDSC. When CS was combined with a single dose of urethane, it led to the development of tumor lesions in lungs within 4 months. By that time, Gr-1+CD11b+ cells accumulated in the spleen and lung, had potent immune suppressive activity and thus can be defined as MDSC. In the CC10Tg model, accumulation of immune suppressive MDSC was observed only at 4 months of age, after the appearance of tumor lesions in lungs. Accumulation of MDSC in both models was abrogated in S100A9 knockout mice. This resulted in a dramatic improvement of survival of mice in both models. Thus, CS results in the expansion of immature myeloid cells lacking suppressive activity. Accumulation of bona fide MDSC in both models was observed only after the development of tumor lesions. However, MDSC played a major role in tumor progression and survival, which suggests that their targeting may provide clinical benefits in lung cancer.

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Section: Introductionsupporting

confidence: 58%

Myeloid-Derived Suppressor Cells in the Development of Lung Cancer

Ortiz

Lu²,

Ramachandran

et al. 2014

Cancer Immunology Research

100

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“…S100A9 was proposed to regulate the antigen-presenting capacity of DCs by modulating co-stimulatory molecule expression in this model. 87 Similarly, S100A9 -/-mice have more severe allergic contact dermatitis. In this case, S100A8 inhibited early DC maturation and antigen presentation in a TLR4-dependent manner.…”

Section: Extracellular Functions and Receptors Of Calgranulinsmentioning

confidence: 99%

Calgranulins May Contribute Vascular Protection In Atherogenesis

Geczy

Chung

Hiroshima

2014

Circ J

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“…Costimulation through the B7/CD28 pathway is important for activation of lymphocytes by alloantigens. S100A9 may modulate tolerogenic dendritic cell-T cell activation by reducing B7 levels and subsequent T-cell priming [237], and its over-expression inhibits dendritic cell differentiation [59]. …”

Section: Extracellular Functions Of S100 Proteinsmentioning

confidence: 99%

Functions of S100 Proteins

Donato¹,

Cannon²,

Sorci³

et al. 2013

Current Molecular Medicine

1,095

709

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The S100 protein family consists of 24 members functionally distributed into three main subgroups: those that only exert intracellular regulatory effects, those with intracellular and extracellular functions and those which mainly exert extracellular regulatory effects. S100 proteins are only expressed in vertebrates and show cell-specific expression patterns. In some instances, a particular S100 protein can be induced in pathological circumstances in a cell type that does not express it in normal physiological conditions. Within cells, S100 proteins are involved in aspects of regulation of proliferation, differentiation, apoptosis, Ca2+ homeostasis, energy metabolism, inflammation and migration/invasion through interactions with a variety of target proteins including enzymes, cytoskeletal subunits, receptors, transcription factors and nucleic acids. Some S100 proteins are secreted or released and regulate cell functions in an autocrine and paracrine manner via activation of surface receptors (e.g. the receptor for advanced glycation end-products and toll-like receptor 4), G-protein-coupled receptors, scavenger receptors, or heparan sulfate proteoglycans and N-glycans. Extracellular S100A4 and S100B also interact with epidermal growth factor and basic fibroblast growth factor, respectively, thereby enhancing the activity of the corresponding receptors. Thus, extracellular S100 proteins exert regulatory activities on monocytes/macrophages/microglia, neutrophils, lymphocytes, mast cells, articular chondrocytes, endothelial and vascular smooth muscle cells, neurons, astrocytes, Schwann cells, epithelial cells, myoblasts and cardiomyocytes, thereby participating in innate and adaptive immune responses, cell migration and chemotaxis, tissue development and repair, and leukocyte and tumor cell invasion.

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Loss of Myeloid Related Protein-8/14 Exacerbates Cardiac Allograft Rejection

Cited by 31 publications

References 59 publications

Myeloid-Derived Suppressor Cells in the Development of Lung Cancer

Myeloid-Derived Suppressor Cells in the Development of Lung Cancer

Calgranulins May Contribute Vascular Protection In Atherogenesis

Functions of S100 Proteins

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