Binding of monomeric immunoglobulins by bone marrow‐derived mononuclear phagocytes; its modulation by interferon‐γ

Keller, R.; Keist, Ruth; Bazin, Hervé; Joller, P.; Vandermeide, Ph.

doi:10.1002/eji.1830200937

Cited by 8 publications

(6 citation statements)

References 18 publications

(10 reference statements)

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“…However, Apcs -/- spleen cells had two discrete populations of spleen cells staining for a common epitope of FcγRII and FcγRIII, whereas spleen cells from C57BL/6 contain a single population (Figure 3C). Rat IgG2b binds to FcγR with high affinity [74], [75]. Compared to C57BL/6 spleen cells, Apcs -/- mice had increased numbers of rat IgG2b-binding spleen cells (Figure 3D).…”

Section: Resultsmentioning

confidence: 99%

Persistent Lung Inflammation and Fibrosis in Serum Amyloid P Component (Apcs-/-) Knockout Mice

Pilling

2014

PLoS ONE

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Fibrosing diseases, such as pulmonary fibrosis, cardiac fibrosis, myelofibrosis, liver fibrosis, and renal fibrosis are chronic and debilitating conditions and are an increasing burden for the healthcare system. Fibrosis involves the accumulation and differentiation of many immune cells, including macrophages and fibroblast-like cells called fibrocytes. The plasma protein serum amyloid P component (SAP; also known as pentraxin-2, PTX2) inhibits fibrocyte differentiation in vitro, and injections of SAP inhibit fibrosis in vivo. SAP also promotes the formation of immuno-regulatory Mreg macrophages. To elucidate the endogenous function of SAP, we used bleomycin aspiration to induce pulmonary inflammation and fibrosis in mice lacking SAP. Compared to wildtype C57BL/6 mice, we find that in Apcs-/- “SAP knock-out” mice, bleomycin induces a more persistent inflammatory response and increased fibrosis. In both C57BL/6 and Apcs-/- mice, injections of exogenous SAP reduce the accumulation of inflammatory macrophages and prevent fibrosis. The types of inflammatory cells present in the lungs following bleomycin-aspiration appear similar between C57BL/6 and Apcs -/- mice, suggesting that the initial immune response is normal in the Apcs-/- mice, and that a key endogenous function of SAP is to promote the resolution of inflammation and fibrosis.

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Section: Resultsmentioning

confidence: 99%

Persistent Lung Inflammation and Fibrosis in Serum Amyloid P Component (Apcs-/-) Knockout Mice

Pilling

2014

PLoS ONE

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“…IFN-g and TNF-a direct B cell maturation, IFN-g drives nonimmunoglobulin-secreting B cells to active immunoglobulin secretion and isotype switches, and affinity maturation [50][51][52][53]. Therefore, the decreased levels of IFN-g and TNF-a may contribute to the production of lower affinity antibodies and the reduced level of AChR-specific IgG2b, which are probably the only isotype triggering antibody-dependent cell-mediated cytotoxicity (ADCC) in rats [54]. These anti-AChR antibodies have less capacity in inducing AChR degradation, and contribute to the partial suppression of disease in rats receiving high-dose AChR.…”

Section: Discussionmentioning

confidence: 99%

Nasal tolerance in experimental autoimmune myasthenia gravis (EAMG): induction of protective tolerance in primed animals

Shi

Bai

et al. 1998

Clinical and Experimental Immunology

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Nasal administration of microg doses of acetylcholine receptor (AChR) is effective in preventing the development of B cell-mediated EAMG in the Lewis rat, a model for human MG. In order to investigate whether nasal administration of AChR modulates ongoing EAMG, Lewis rats were treated nasally with AChR 2 weeks after immunization with AChR and Freund's complete adjuvant. Ten-fold higher amounts of AChR given nasally (600 microg/rat) were required to ameliorate the manifestations of EAMG compared with the amounts necessary for prevention of EAMG. In lymph node cells from rats receiving 600 microg/rat of AChR, AChR-induced proliferation and interferon-gamma (IFN-gamma) secretion were reduced compared with control EAMG rats receiving PBS only. The anti-AChR antibodies in rats treated nasally with 600 microg/rat of AChR had lower affinity, reduced proportion of IgG2b and reduced capacity to induce AChR degradation. Numbers of AChR-reactive IFN-gamma and tumour necrosis factor-alpha (TNF-alpha) mRNA-expressing lymph node cells from rats treated nasally with 600 microg/rat of AChR were suppressed, while IL-4, IL-10 and transforming growth factor-beta (TGF-beta) mRNA-expressing cells were not affected. Collectively, these data indicate that nasal administration of AChR in ongoing EAMG induced selective suppression of Th1 functions, i.e. IFN-gamma and IgG2b production, but no influence on Th2 cell functions. The impaired Th1 functions may result in the production of less myasthenic anti-AChR antibodies and contribute to the amelioration of EAMG severity in rats treated with AChR 600 microg/rat by the nasal route.

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“…There is ample evidence for the regulatory effects of IFN-y alone or in combination with other cytokines or cells, on B cell function and differentiation (Jurado er al. 1989, Michael et al 1989, Keller et al 1990, Snapper 1990, Nakagawa et al 1992. In this light, and if T. cruzi affected IFN-yR expression by B cells in infected hosts as it did in our co-culture system, the effect reported herein would be anticipated to contribute to B cell dysfunction and immunosuppression, i.e.…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma cruz/‐induced decrease in the level of interferon‐7 receptor expression by resting and activated human blood lymphocytes

Kierszenbaum

López

Tanner

et al. 1995

Parasite Immunology

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A substantial proportion of human peripheral blood mononuclear cells (PBMC) manifested a decreased capacity to express membrane interferon-gamma receptors (IFN-gamma R) when co-cultured with Trypanosoma cruzi. Among the lymphocytes, B cells accounted for the bulk of this effect, evidenced by a marked drop in the proportion of CD19+ or CD20+ cells expressing IFN-gamma R. Decreased IFN-gamma R expression by B lymphocytes was seen as early as 3 h after co-culture with T. cruzi and persisted for at least 24 h. The parasite had no detectable effect on CD19, CD20 or DR antigen expression by B lymphocytes. Neither the proportion of B cells expressing these markers nor the membrane density of these molecules varied significantly in the presence of T. cruzi. In PBMC cultures stimulated with Staphlyococcus aureus Cowan I (SACI), T. cruzi decreased the percentages of both IFN-gamma R+ and IFN-R+bright (cells expressing above-normal levels of surface IFN-gamma R) B lymphocytes. Cell-free filtrates of T. cruzi suspensions reproduced the suppressive effects of living parasites on IFN-gamma R expression by B cells. When T. cruzi present, the intracellular levels of IFN-gamma R molecules in resting or SACI-activated B lymphocytes, represented by fluorescence intensity, were well below control values, suggesting that decreased surface expression resulted from suppressed IFN-gamma R synthesis. Among T (CD3+) cells, 10.8% to 39.6% (7 donors) expressed surface IFN-gamma R and did so at a very low level. These percentages were also reduced by T. cruzi.(ABSTRACT TRUNCATED AT 250 WORDS)

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Binding of monomeric immunoglobulins by bone marrow‐derived mononuclear phagocytes; its modulation by interferon‐γ

Cited by 8 publications

References 18 publications

Persistent Lung Inflammation and Fibrosis in Serum Amyloid P Component (Apcs-/-) Knockout Mice

Persistent Lung Inflammation and Fibrosis in Serum Amyloid P Component (Apcs-/-) Knockout Mice

Nasal tolerance in experimental autoimmune myasthenia gravis (EAMG): induction of protective tolerance in primed animals

Trypanosoma cruz/‐induced decrease in the level of interferon‐7 receptor expression by resting and activated human blood lymphocytes

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