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. 2010 Nov 9;107(45):19396-401.
doi: 10.1073/pnas.1014515107. Epub 2010 Oct 25.

VSports注册入口 - FcγRIV deletion reveals its central role for IgG2a and IgG2b activity in vivo

Falk Nimmerjahn  1 , Anja Lux, Heike Albert, Melissa Woigk, Christian Lehmann, Diana Dudziak, Patrick Smith, Jeffrey V Ravetch
Affiliations

FcγRIV deletion reveals its central role for IgG2a and IgG2b activity in vivo

"V体育平台登录" Falk Nimmerjahn et al. Proc Natl Acad Sci U S A. .

VSports在线直播 - Abstract

Cellular Fcγ receptors are essential for IgG-dependent effector functions in vivo. There is convincing evidence that selective activating Fcγ receptors are responsible for the activity of individual IgG subclasses. Thus, IgG1 activity is absent in FcγRIII-deficient mice, and several studies suggest that the activity of the most potent IgG subclasses, IgG2a and IgG2b, might be dependent on either individual or a combination of activating FcγRs. To study the role of individual activating FcγRs for IgG subclass activity, we generated an FcγRIV-deficient mouse and showed that a variety of IgG2a- and IgG2b-dependent effector functions are impaired in the absence of this activating Fc receptor in models of autoimmunity and antibody-dependent cellular cytotoxicity VSports手机版. .

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Conflict of interest statement

The authors declare no conflict of interest.

"VSports app下载" Figures

Fig. 1.
Fig. 1.
Characterization of the FcγRIV knockout mouse. (A) Analysis of FcγRIV expression (anti-FcγRIV) on granulocytes (identified by Ly6G expression) and monocytes (identified by CD11b expression) in the blood. (B) Expression of FcγRIV on granulocytes and monocytes in the blood, spleen, and bone marrow of C57BL/6 and FcγRIV knockout mice. (C) Immunohistochemical analysis of FcγRIV expression on splenic macrophages in C57BL/6 and FcγRIV knockout animals. B-cells were identified by staining with B220. (D) The expression level of activating FcγRIII and FcγRIV in C57BL/6 (solid bars), FcγRIII (open bars), and FcγRIV (hatched bars) knockout mice on neutrophils in the blood.
Fig. 2.
Fig. 2.
Role of FcγRIV in IgG2a-mediated killing of s.c. melanoma cells. C57BL/6, FcγRI−/−, FcγRIII−/−, FcγRIV, and FcγRI/III−/− mice (n = 5) were injected subcutaneously with B16F10 melanoma cells followed by treatment with the therapeutic TA99-IgG2a antibody specific for mouse gp75 (TA99-IgG2a) or PBS as a control. The tumor size over time in the indicated mouse strains is graphed.
Fig. 3.
Fig. 3.
Role of FcγRIV in the Arthus and PCA reaction. C57BL/6 and FcγRIV knockout mice were injected intradermally with rabbit anti-OVA IgG or PBS followed by i.v. administration of ovalbumin in Evans blue. Shown is edema formation at the sites of IgG deposition (A) and the area (B) of dye influx into the skin in the indicated mouse strains. (C) The indicated mouse strains received an injection of mouse IgE anti-DNP intradermally into the ear followed by systemic administration of DNP-human serum albumin (HSA) in Evans blue 12 h later. Shown is the edema formation 60 min after DNP-HSA injection in one representative of four animals per group. (D) Quantification of edema formation in C57BL/6-, FcγRIV-, and FcR γ-chain–deficient mice by calculating the percentage of the ear area affected by the edema.
Fig. 4.
Fig. 4.
Role of FcγRIV in rheumatoid arthritis. (A) The development of clinical signs of arthritis in C57BL/6 and FcγRIV knockout mice upon injection of KBxN serum. (B) Measurement of the area of immigrated innate immune effector cells into the joints of C57BL/6 and FcγRIV knockout animals (n = 4). An asterisk in A and B indicates a significant difference with a p-value less than 0.05. (C) Histological analysis of inflamed joints of C57BL/6 and FcγRIV knockout animals. (D) Detection of IgG subclass anti-GPI autoantibodies in the serum of KBxN mice.
Fig. 5.
Fig. 5.
Role of FcγRIV in a model of nephrotoxic nephritis. The indicated mouse strains were immunized with sheep IgG followed by injection of sheep nephrotoxic serum. (A) Detection of IgG2b mouse anti-sheep antibodies 2 wk after immunization of the indicated mouse strains with sheep IgG. (B) The blood urea nitrogen level (BUN) in C57BL/6- and FcγRIV-deficient mice before and 4 d after injection of nephrotoxic serum. (C) Detection of fibrotic tissue in the kidneys of C57BL/6- and FcγRIV-deficient mice 4 d after injection of nephrotoxic serum by staining with sirius red. In all experiments, four mice per group were used.
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References

    1. Hogarth PM. Fc receptors are major mediators of antibody based inflammation in autoimmunity. Curr Opin Immunol. 2002;14:798–802. - V体育官网入口 - PubMed
    1. Nimmerjahn F, Ravetch JV. Antibody-mediated modulation of immune responses. Immunol Rev. 2010;236:265–275. - PubMed
    1. Takai T. Roles of Fc receptors in autoimmunity. Nat Rev Immunol. 2002;2:580–592. - PubMed
    1. Nimmerjahn F, Ravetch JV. Fcgamma receptors as regulators of immune responses. Nat Rev Immunol. 2008;8:34–47. - PubMed
    1. Ravetch JV, Clynes RA. Divergent roles for Fc receptors and complement in vivo. Annu Rev Immunol. 1998;16:421–432. - PubMed

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