IgG-mediated anaphylaxis via Fcγ receptor in CD40-deficient mice

Wakayama, Hisashi; Hasegawa, Yoshinori; Kawabe, Tsutomu; Saito, Hidehiko; Kikutani, Hitoshi; Shimokata, Kaoru

doi:10.1046/j.1365-2249.1998.00717.x

Cited by 12 publications

(6 citation statements)

References 29 publications

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“…We conclude that Fc + R plays a central role in triggering anti-GBM antibody-mediated glomerulonephritis as a representative type II hypersensitivity disease. We recently demonstrated the inflammatory pathway of IgGmediated immediate hypersensitivity reaction and its triggering mechanism through Fc + R in in vivo conditions [39]. Taking previous findings and the present results into consideration, we suggest that Fc + R may play the key role in triggering IgG-mediated inflammatory reactions even in the in vivo condition.…”

Section: Discussionsupporting

confidence: 81%

Abolition of anti-glomerular basement membrane antibody-mediated glomerulonephritis in FcRγ-deficient mice

et al. 2000

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Several recent studies have demonstrated the central role of Fc receptors (FcR) rather than the complement system in triggering hypersensitivity reactions. We investigated the role of FcR for IgG (FcγR) using a murine model of accelerated anti‐glomerular basement membrane (GBM) antibody‐mediated glomerulonephritis as a representative of type II hypersensitivity diseases. Intravenous injection of rabbit anti‐GBM antibody after preimmunization with normal rabbit IgG induced proteinuria and azotemia in wild‐type C57BL / 6 and CD40+ / – mice but not in FcR γ chain (FcRγ)– / – mice or CD40– / – mice. Light microscopic findings revealed marked tissue damage in the glomeruli of wild‐type C57BL / 6 and CD40+ / – mice. However, no tissue damage except polymorphonuclear cell infiltration was observed in the glomeruli of FcRγ– / – mice. The glomeruli of CD40– / – mice were almost normal. Immunohistochemistry revealed the binding of rabbit IgG to the GBM in all mice injected with anti‐GBM antibody. However, depositions of mouse IgG and complement to the glomeruli were not observed in CD40– / – mice, and deposition of fibrin was not observed in FcRγ– / – or CD40– / – mice. These findings suggest that FcγR may initiate anti‐GBM antibody‐mediated renal disease. We conclude that FcγR rather than the complement system is critically involved in the development of type II hypersensitivity diseases.

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Section: Discussionsupporting

confidence: 81%

Abolition of anti-glomerular basement membrane antibody-mediated glomerulonephritis in FcRγ-deficient mice

et al. 2000

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“…Anaphylaxis in mice can be brought about not only by an IgE-Fc∊RI mechanism but also through an IgG-FcγR interaction 3 , 4 , 7 , 29 ; therefore, we hypothesized that the decreased expression of CD200R3 was induced by FcγR-mediated stimulation. This hypothesis was strongly supported by the following findings: (i) CD200R3 on basophils sensitized with IgG-depleted antiserum was not down-regulated following specific antigen challenge ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Decreased expression of CD200R3 on mouse basophils as a novel marker for IgG1‐mediated anaphylaxis

Iwamoto

Matsubara

Nakazato

et al. 2015

Immunity Inflam & Disease

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IgE-mediated mast cell activation is the trigger of anaphylaxis in humans, whereas it is known that not only IgE but also IgG can induce anaphylaxis in mice. In our preliminary experiments, the expression of a murine basophil identification marker, CD200R3, on antigen-sensitized basophils decreased following specific antigen challenge. Interestingly, this decrease did not always correspond with increased expression of the IgE-mediated basophil activation marker CD200R1. Since IgG as well as IgE plays a role in mouse anaphylaxis, we hypothesized that the observed decrease in CD200R3 on basophils was caused by IgG-mediated cell activation. We attempted to establish whether CD200R3 is a marker of IgG-mediated basophil activation and if its expression is correlated with anaphylaxis in a mouse model. Mouse basophils were stimulated via Fc∊Rs and/or FcγRs, and levels of CD200R1 and CD200R3 were analyzed by flow cytometry. Basophils derived from naive mice were challenged with a natural antigen, β-lactoglobulin, after passive sensitization with anti-β-LG serum or IgG/IgG subclass-depleted antiserum. Systemic anaphylaxis was induced by i.v. injection of anti-FcγRIII/II monoclonal antibody, and CD200R3 expression on peripheral basophils was assessed. Stimulation via Fc∊Rs induced a significant increase in CD200R1 expression but had only a small effect on that of CD200R3. However, anti-FcγRIII/II stimulation reduced CD200R3 expression markedly. In passive sensitization experiments, down-regulation of CD200R3 induced by antigen challenge was strongly negated by the depletion of IgG or IgG1 from antiserum. Intravenous injection of anti-FcγRIII/II induced CD200R3 down-regulation on peripheral basophils, together with a drop in rectal temperature. Lowered CD200R3 expression on basophils is induced by IgG-mediated stimulation via FcγRs. Use of CD200R1 and CD200R3 as activation markers enables the evaluation of murine basophil activation mediated by IgE and IgG, respectively.

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“…Nevertheless, IgE-de®cient mice can develop anaphylactic responses (Oettgen et al 1994), possibly mediated by IgG antibody. IgG can bind to Fcc in vivo and trigger degranulation (Wakayama et al 1998). During nematode infection, eosinophils demonstrate morphological signs of degranulation and an increase in the number of Fcc receptors (Winqvist et al 1982;Weller 1991).…”

Section: Introductionmentioning

confidence: 99%

Immune response to Trichinella spiralis larvae after treatment with the anti-allergic compound ketotifen

Doligalska¹

2000

Parasitology Research

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Ketotifen was used as an anti-allergic agent to study the relationship between eosinophil-related responses and IgG1 and IgG2a antibody responses in BALB/c mice infected with Trichinella spiralis. The results showed that leukocyte and eosinophil numbers and interleukin-5 (IL-5) concentrations in the peritoneal fluid increased after exposure to nematodes and the increases were slightly greater in animals treated with ketotifen. A decreased concentration of eosinophil peroxidase and an elevation in IgG1 accompanied the muscle phase of infection. In mice treated with ketotifen, antibody-mediated recognition of muscle larvae was delayed. The retardation of IgG1 and IgG2a responses may have been responsible for the ineffective immune response against larvae migrating into the muscle. The activation of eosinophils was accompanied by changes in IL-5 concentration, but these changes were not associated with differences in protection against infection.

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IgG-mediated anaphylaxis via Fcγ receptor in CD40-deficient mice

Cited by 12 publications

References 29 publications

Abolition of anti-glomerular basement membrane antibody-mediated glomerulonephritis in FcRγ-deficient mice

Abolition of anti-glomerular basement membrane antibody-mediated glomerulonephritis in FcRγ-deficient mice

Decreased expression of CD200R3 on mouse basophils as a novel marker for IgG1‐mediated anaphylaxis

Immune response to Trichinella spiralis larvae after treatment with the anti-allergic compound ketotifen

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