Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor 1.

Hora, K.; Satriano, Joseph; Santiago, Arthur; Mori, Tetsuo; Stanley, E. Richard; Shan, Zihe; Schlöndorff, Detlef

doi:10.1073/pnas.89.5.1745

Cited by 105 publications

(59 citation statements)

References 31 publications

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“…Mesangial cells play an important role in inflammation in the kidney (59,60). Interaction of ICs with mesangial cells via Fc receptors triggers a cascade of renal injury characterized by cellular proliferation, matrix protein accumulation, chemokine release, and mononuclear cell recruitment (56,(61)(62)(63)(64)(65). A recent study of lupus-prone mice (NZB/ NZW F 1 mice) deficient for Fc receptor ␥-chain I and III expression (Fc␥RI and Fc␥RIII) indicated that the presence of Fc␥Rs was required for development of proliferative glomerulonephritis (66).…”

Section: Discussionmentioning

confidence: 99%

Complement Component C3 Is Not Required for Full Expression of Immune Complex Glomerulonephritis in MRL/lprMice

Sekine

Reilly

Molano

et al. 2001

The Journal of Immunology

134

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Complement activation and tissue deposition of complement fragments occur during disease progression in lupus nephritis. Genetic deficiency of some complement components (e.g., Factor B) and infusion of complement inhibitors (e.g., Crry, anti-C5 Ab) protect against inflammatory renal disease. Paradoxically, genetic deficiencies of early components of the classical complement pathway (e.g., C1q, C4, and C2) are associated with an increased incidence of lupus in humans and lupus-like disease in murine knockout strains. Complement protein C3 is the converging point for activation of all three complement pathways and thus plays a critical role in biologic processes mediated by complement activation. To define the role of C3 in lupus nephritis, mice rendered C3 deficient by targeted deletion were backcrossed for eight generations to MRL/lpr mice, a mouse strain that spontaneously develops lupus-like disease. We derived homozygous knockout (C3−/−), heterozygous (C3+/−), and C3 wild-type (C3+/+) MRL/lpr mice. Serum levels of autoantibodies and circulating immune complexes were similar among the three groups. However, there was earlier and significantly greater albuminuria in the C3−/− mice compared with the other two groups. Glomerular IgG deposition was also significantly greater in the C3−/− mice than in the other two groups, although overall pathologic renal scores were similar. These results indicate that C3 and/or activation of C3 is not required for full expression of immune complex renal disease in MRL/lpr mice and may in fact play a beneficial role via clearance of immune complexes.

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Section: Discussionmentioning

confidence: 99%

Complement Component C3 Is Not Required for Full Expression of Immune Complex Glomerulonephritis in MRL/lprMice

Sekine

Reilly

Molano

et al. 2001

The Journal of Immunology

134

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“…A characteristic feature of GN is the infiltration of leucocytes from the circulation into the kidney tissue, and the subsequent activation of such inflammatory cells at the site of glomerular injury. It has been demonstrated that mesangial cells are a rich source of chemokines attracting different leucocyte populations into the glomerulus [10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

IFNγ induces functional chemokine receptor expression in human mesangial cells

Schwarz

Wahl

Resch

et al. 2002

Clinical and Experimental Immunology

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SUMMARY Infiltration of leucocyte populations into sites of inflammation is a common feature in renal diseases. Glomerular mesangial cells are potent producers of a variety of chemokines, leading to specific attraction of distinct types of inflammatory leucocytes into the glomerulus, but so far there is limited knowledge about the responsiveness of mesangial cells to chemokines. We investigated the expression of chemokine receptors and the responsiveness of primary human mesangial cells (HMC) to the chemokines which they produce, namely monocyte chemoattractant protein-1 (MCP-1) and interleukin (IL)-8. We found that mRNAs of the chemokine receptors CCR1, which has been shown before, CCR2 and CXCR2 were induced by T-helper cytokine interferon-gamma (IFNγ). In IFNγ-stimulated cells, CCR2 and CXCR2 were detectable by flow cytometry. Following treatment with IFNγ, HMC responded to MCP-1 and IL-8 with an increase of IL-6 mRNA and protein expression, which was in part blocked by pertussis toxin. Moreover, chemokine stimulation of transfected HMC led to an activation of the immunoregulatory transcription factors NFκB and AP-1. Additionally, we found that MCP-1 enhanced the expression of its own mRNA in cells activated to express CCR2, suggesting autocrine feedback mechanisms in MCP-1 regulation. Finally, IFNγ-activated cells migrated towards an MCP-1 gradient in a chemotaxis assay. These results strengthen the assumption that chemokines are not only involved in the recruitment of immune cells to inflamed tissues, but also seem to play a central role in the autocrine regulation of local tissue cells, leading to proceeding inflammation and possibly contributing to healing by mediating cell growth and migration.

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“…MCs are known to take up large particles, including immune complexes (Hora et al 1992). Phagocytosis is receptor-and actin-dependent.…”

Section: Impact Of Lipid Accumulation On Phagocytosismentioning

confidence: 99%

“…MCs are known to phagocytose both particulate matter and immune complexes (Hora et al 1992), which mediate intraglomerular inflammation and limit glomerular injury. In previous short-term studies, IGF-1 treatment enhanced fluid-phase pinocytosis and membrane turnover , which would be expected to enhance phagocytosis.…”

Section: Altered Phagocytosis and Cytoskeletal Reorganizationmentioning

confidence: 99%

IGF-1 Induces Foam Cell Formation in Rat Glomerular Mesangial Cells

Berfield

Abrass

2002

J Histochem Cytochem.

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Veteran Affairs Puget Sound Health Care System, Seattle, Washington S U M M A R Y When rat glomerular mesangial cells (MCs) are cultured with IGF-1 they accumulate intracellular lipid and take on foam cell morphology. These changes were characterized by electron microscopy and Nile red staining. To define the mechanism responsible for IGF-1-mediated lipid uptake, MCs were evaluated for endocytosis, scavenger receptor activity, and receptor-mediated uptake by the LDL receptor. Lipid accumulation was markedly increased when MCs were cultured with IGF. The primary route of uptake was through enhanced endocytosis. Lipid-laden MCs have decreased phagocytic capacity and disrupted cytoskeletons. These data show that IGF-1 induces MC to take on a foam cell morphology and that lipidladen MCs have impaired phagocytic function.

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Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor 1.

Cited by 105 publications

References 31 publications

Complement Component C3 Is Not Required for Full Expression of Immune Complex Glomerulonephritis in MRL/lprMice

Complement Component C3 Is Not Required for Full Expression of Immune Complex Glomerulonephritis in MRL/lprMice

IFNγ induces functional chemokine receptor expression in human mesangial cells

IGF-1 Induces Foam Cell Formation in Rat Glomerular Mesangial Cells

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