Colony-Stimulating Factor-1-Dependent Macrophages Are Responsible for IVIG Protection in Antibody-Induced Autoimmune Disease

The ability of IVIG to induce expression of FcγRIIB and thereby prevent antibody-induced inflammation has been used as a probe to dissect the effector cell components in the KRNxNOD (K/BxN) arthritis model. IVIG protection resulted from the induction of FcγRIIB on infiltrating macrophages but not ne...

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Published inImmunity (Cambridge, Mass.) Vol. 18; no. 4; pp. 573 - 581
Main Authors Bruhns, Pierre, Samuelsson, Astrid, Pollard, Jeffrey W, Ravetch, Jeffrey V
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.04.2003
Elsevier Limited
Elsevier
Subjects
Animals
Ankle
Arthritis
Arthritis - prevention & control
Autoantibodies
Autoantibodies - immunology
Autoimmune Diseases
Autoimmune Diseases - prevention & control
Cytotoxicity
Disease
Histology
Immune system
Immunoglobulins, Intravenous
Immunoglobulins, Intravenous - therapeutic use
Immunology
Life Sciences
Macrophage Colony-Stimulating Factor
Macrophage Colony-Stimulating Factor - physiology
Macrophages
Macrophages - physiology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Inbred NOD
Purpura, Thrombocytopenic, Idiopathic
Purpura, Thrombocytopenic, Idiopathic - prevention & control
Receptors, IgG
Receptors, IgG - biosynthesis
Rodents
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Summary:The ability of IVIG to induce expression of FcγRIIB and thereby prevent antibody-induced inflammation has been used as a probe to dissect the effector cell components in the KRNxNOD (K/BxN) arthritis model. IVIG protection resulted from the induction of FcγRIIB on infiltrating macrophages but not neutrophils, indicating a critical role for macrophage activation in this disease model. Disease induction but not IVIG protection was observed in CSF-1-deficient mice ( op/op) in K/BxN arthritis, thus defining different macrophage subsets in these processes. These results suggest a two-step model for IVIG protection in which CSF-1-dependent macrophages act as innate “sensors” for the Fc fragment of IVIG, leading to the induction of FcγRIIB on CSF-1-independent “effector” macrophages thereby raising the threshold required for FcγRIII activation and preventing autoantibody-triggered inflammation.
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ISSN:1074-7613
1097-4180
DOI:10.1016/S1074-7613(03)00080-3