Complement activation selectively potentiates the pathogenicity of the IgG2b and IgG3 isotypes of a high affinity anti-erythrocyte autoantibody

Journal of Experimental Medicine

Volumn 195, Issue 6, 2002, Pages 665-672

  Da Silveira, Samareh Azeredo ^a   Kikuchi, Shuichi ^a   Fossati Jimack, Liliane ^b   Moll, Thomas ^a   Saito, Takashi ^c   Sjef Verbeek, J ^d   Botto, Marina ^b   Walport, Mark J ^b   Carroll, Michael ^e   Izui, Shozo ^a,f  

^a UNIVERSITY OF GENEVA   (Switzerland)

^b IMPERIAL COLLEGE SCHOOL OF MEDICINE   (United Kingdom)

^c CHIBA UNIVERSITY   (Japan)

^d LEIDEN UNIVERSITY MEDICAL CENTER   (Netherlands)

^e HARVARD MEDICAL SCHOOL   (United States)

^f CMU   (Switzerland)

Author keywords

Autoimmune hemolytic anemia; Complement receptor; Fc receptor; IgG isotype; Phagocytosis

Indexed keywords

AUTOANTIBODY; COMPLEMENT COMPONENT C3; ERYTHROCYTE ANTIBODY; FC RECEPTOR; IMMUNOGLOBULIN G1; IMMUNOGLOBULIN G2A; IMMUNOGLOBULIN G2B; IMMUNOGLOBULIN G3; MONOCLONAL ANTIBODY;

ANIMAL MODEL; ANTIGEN BINDING; ARTICLE; AUTOIMMUNE HEMOLYTIC ANEMIA; AUTOIMMUNITY; BINDING AFFINITY; COMPLEMENT ACTIVATION; COMPLEMENT SYSTEM; ENZYME LINKED IMMUNOSORBENT ASSAY; ERYTHROCYTE; EXPERIMENTAL MODEL; FLOW CYTOMETRY; HEMOLYSIS; HEMOLYTIC ANEMIA; MOUSE; NONHUMAN; PRIORITY JOURNAL;

ANEMIA, HEMOLYTIC, AUTOIMMUNE; ANIMALS; AUTOANTIBODIES; COMPLEMENT ACTIVATION; ERYTHROCYTES; IMMUNOGLOBULIN CLASS SWITCHING; IMMUNOGLOBULIN G; MICE; MICE, INBRED BALB C; RECEPTORS, IGG;

EID: 0037128658     PISSN: 00221007     EISSN: None     Source Type: Journal    
DOI: 10.1084/jem.20012024     Document Type: Article

References (39)

1. High pathogenic potential of low-affinity autoantibodies in experimental autoimmune hemolytic anemia
2. Markedly different pathogenicity of four IgG isotype-switch variants of an anti-erythrocyte autoantibody is based on their respective capacity to interact in vivo with the low-affinity FcγRIII
3. Monoclonal anti-enthrocyte autoantibodies derived from NZB mice cause autoimmune hemolytic anemia by two distinct pathogenic mechanisms
4. Cytotoxic antibodies trigger inflammation through Fc receptors
5. FcγRIII (CD16)-deficient mice show IgG isotope-dependent protection to experimental autoimmune hemolytic anemia
6. Fc receptors: Rubor redux
7. FcR γ chain deletion results in pleiotrophic effector cell defects
8. Immunoglobulin G-mediated inflammatory responses develop normally in complement deficient mice
9. Activation of mouse complement by different classes of mouse antibody
10. Activation of mouse complement by monoclonal mouse antibodies
11. Role of antibody and complement in the immune clearance and destruction of erythrocytes. I. In vivo effects of IgG and IgM complement-fixing sites
12. Resistance of Fc receptor-deficient mice to fatal glomerulonephritis
13. Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies
14. Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity
15. A B cell-deficient mouse by targeted disruption of the membrane exon of the immunoglobulin μ chain gene
16. Expression and regulation of immunoglobulin heavy gene transfected into lymphoid cells
17. "Enhancer-constitutive" vectors for the expression of recombinant antibodies
18. Complete nucleotide sequence of immunoglobulin γ2b chain gene cloned from newborn mouse DNA
19. Structural analysis of the murine IgG3 constant region gene
20. A new mouse immunoglobulin: IgG3
21. Murine IgG1 complexes trigger immune effector functions predominantly via FcγRIII (CD16)
22. Identification of the mouse IgG3 receptor: Implications for antibody effector function at the interface between innate and adaptive immunity
23. Binding of monomeric immunoglobulins to Fc receptors of mouse macrophages
24. Binding and activation of C1 by cell bound IgG: Activation depends on cell surface hapten density
25. Mouse monoclonal antibodies at the red cell surface. II. Effect of hapten density on complement fixation and activation
26. Mechanism of inhibition of immunoglobulin G-mediated phagocytosis by monoclonal antibodies that recognize the Mac-1 antigen
27. CR3 and FcγRIII cooperate in generation of a neutrophil respiratory burst: Requirement for FcγRII and tyrosine phosphorylation
28. A new Fc receptor on mouse macrophages binding IgG3
29. Antibody-mediated modulation of Cryptococcus neoformans infection is dependent on distinct Fc receptor functions and IgG subclasses
30. Anti-inflammatory activity of IVIG mediated through the inhibitory receptor
31. Fc receptors initiate the Arthus reaction: Redefining the inflammatory cascade
32. Modulation of immune complex-induced inflammation in vivo by the coordinate expression of activation and inhibitory Fc receptors
33. Impaired inflammatory responses in the reverse Arthus reaction through genetic deletion of the C5a receptor
34. Impaired IgG-dependent anaphylaxis and Arthus reaction in FcγRIII (CD16) deficient mice
35. A codominant role of FcγRI/III and C5aR in the reverse Arthus reaction
36. Neurogenic amplification of immune complex inflammation
37. A role of Mac-1(CD11b/CD18) in immune complex-stimulated neutrophil function in vivo: Mac-1 deficiency abrogates sustained Fcγ receptor-dependent neutrophil adhesion and complement-dependent proteinuria in acute glomerulonephritis
38. Impaired mast cell-dependent natural immunity in complement C3 deficient mice
39. The C5a chemoattractant receptor mediates mucosal defence to infection