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Immunoglobulin G-mediated inflammatory responses develop normally in complement-deficient mice.

Sylvestre D, Clynes R, Ma M, Warren H, Carroll MC, Ravetch JV - J. Exp. Med. (1996)

Bottom Line: Complement-deficient and wild-type animals exhibit comparable levels of erythrophagocytosis and platelet clearance in response to cytotoxic anti-red blood cell and antiplatelet antibodies.Furthermore, in the reverse passive Arthus reaction, soluble immune complexes induce equivalent levels of hemmorhage, edema, and neutrophillic infiltration in complement-deficient and wild-type animals.In contrast, mice that are genetically deficient in the expression of Fc receptors exhibit grossly diminished reactions by both cytotoxic antibodies and soluble immune complexes.

View Article: PubMed Central - PubMed

Affiliation: Division of Molecular Biology, Memorial Sloan-Kettering Cancer Center, New York 10021, USA.

ABSTRACT
The role of complement in immunoglobulin G-triggered inflammation was studied in mice genetically deficient in complement components C3 and C4. Using the reverse passive Arthus reaction and experimental models of immune hemolytic anemia and immune thrombocytopenia, we show that these mice have types II and III inflammatory responses that are indistinguishable from those of wild-type animals. Complement-deficient and wild-type animals exhibit comparable levels of erythrophagocytosis and platelet clearance in response to cytotoxic anti-red blood cell and antiplatelet antibodies. Furthermore, in the reverse passive Arthus reaction, soluble immune complexes induce equivalent levels of hemmorhage, edema, and neutrophillic infiltration in complement-deficient and wild-type animals. In contrast, mice that are genetically deficient in the expression of Fc receptors exhibit grossly diminished reactions by both cytotoxic antibodies and soluble immune complexes. These studies provide strong evidence that the activation of cell-based Fc gamma R receptors, but not complement, are required for antibody-triggered murine inflammatory responses.

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Quantitation of 8-h  neutrophil infiltration in the reverse passive Arthus reaction. (A)  30 mg of rabbit IgG (upper left spot)  or rabbit anti-OVA IgG was injected intradermally, followed by 2  mg/kg i.v. OVA. Dorsal skins  were harvested after 8 h. (B) Aggregated results based on the direct  microscopic grading of neutrophil  infiltration on a scale of 0–4+.  Results are ± SD; n >12 in each  group.
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Figure 3: Quantitation of 8-h neutrophil infiltration in the reverse passive Arthus reaction. (A) 30 mg of rabbit IgG (upper left spot) or rabbit anti-OVA IgG was injected intradermally, followed by 2 mg/kg i.v. OVA. Dorsal skins were harvested after 8 h. (B) Aggregated results based on the direct microscopic grading of neutrophil infiltration on a scale of 0–4+. Results are ± SD; n >12 in each group.

Mentions: Fig. 3 A shows representative histological sections from an 8-h Arthus reaction in wild-type (left), C3−/− (center), and FcR−/− (right) mice. Once again, a vigorous neutrophil infiltration is observed in the C3 knockout animals and wild-type controls, with FcR-deficient mice exhibiting a near absence of infiltrating cells. C4-deficient mice and DBA/2 mice (not shown) were able to recruit neutrophils, as were wild-type or C3deficient mice. Quantitation by microscopy (Fig. 3 B) or MPO activity (data not shown) reveals that only FcR-deficient mice have a reduction in this parameter.


Immunoglobulin G-mediated inflammatory responses develop normally in complement-deficient mice.

Sylvestre D, Clynes R, Ma M, Warren H, Carroll MC, Ravetch JV - J. Exp. Med. (1996)

Quantitation of 8-h  neutrophil infiltration in the reverse passive Arthus reaction. (A)  30 mg of rabbit IgG (upper left spot)  or rabbit anti-OVA IgG was injected intradermally, followed by 2  mg/kg i.v. OVA. Dorsal skins  were harvested after 8 h. (B) Aggregated results based on the direct  microscopic grading of neutrophil  infiltration on a scale of 0–4+.  Results are ± SD; n >12 in each  group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196366&req=5

Figure 3: Quantitation of 8-h neutrophil infiltration in the reverse passive Arthus reaction. (A) 30 mg of rabbit IgG (upper left spot) or rabbit anti-OVA IgG was injected intradermally, followed by 2 mg/kg i.v. OVA. Dorsal skins were harvested after 8 h. (B) Aggregated results based on the direct microscopic grading of neutrophil infiltration on a scale of 0–4+. Results are ± SD; n >12 in each group.
Mentions: Fig. 3 A shows representative histological sections from an 8-h Arthus reaction in wild-type (left), C3−/− (center), and FcR−/− (right) mice. Once again, a vigorous neutrophil infiltration is observed in the C3 knockout animals and wild-type controls, with FcR-deficient mice exhibiting a near absence of infiltrating cells. C4-deficient mice and DBA/2 mice (not shown) were able to recruit neutrophils, as were wild-type or C3deficient mice. Quantitation by microscopy (Fig. 3 B) or MPO activity (data not shown) reveals that only FcR-deficient mice have a reduction in this parameter.

Bottom Line: Complement-deficient and wild-type animals exhibit comparable levels of erythrophagocytosis and platelet clearance in response to cytotoxic anti-red blood cell and antiplatelet antibodies.Furthermore, in the reverse passive Arthus reaction, soluble immune complexes induce equivalent levels of hemmorhage, edema, and neutrophillic infiltration in complement-deficient and wild-type animals.In contrast, mice that are genetically deficient in the expression of Fc receptors exhibit grossly diminished reactions by both cytotoxic antibodies and soluble immune complexes.

View Article: PubMed Central - PubMed

Affiliation: Division of Molecular Biology, Memorial Sloan-Kettering Cancer Center, New York 10021, USA.

ABSTRACT
The role of complement in immunoglobulin G-triggered inflammation was studied in mice genetically deficient in complement components C3 and C4. Using the reverse passive Arthus reaction and experimental models of immune hemolytic anemia and immune thrombocytopenia, we show that these mice have types II and III inflammatory responses that are indistinguishable from those of wild-type animals. Complement-deficient and wild-type animals exhibit comparable levels of erythrophagocytosis and platelet clearance in response to cytotoxic anti-red blood cell and antiplatelet antibodies. Furthermore, in the reverse passive Arthus reaction, soluble immune complexes induce equivalent levels of hemmorhage, edema, and neutrophillic infiltration in complement-deficient and wild-type animals. In contrast, mice that are genetically deficient in the expression of Fc receptors exhibit grossly diminished reactions by both cytotoxic antibodies and soluble immune complexes. These studies provide strong evidence that the activation of cell-based Fc gamma R receptors, but not complement, are required for antibody-triggered murine inflammatory responses.

Show MeSH
Related in: MedlinePlus