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© Matteo Bonazzi, Edith Gouin
Observation en immunofluorescence d'une cellule infectée par Listeria monocytogenes. En bleu: marquage des protéines de surface de Listeria qui permet de visualiser les bactéries. En rouge et vert: marquage de l'actine, une protéine qui forme le cytosquelette des cellules. Les Listeria utilisent l'actine cellulaire pour former des "comêtes" et se déplacer à l'intérieur des cellules qu'elles infectent. Cell infected by Listeria monocytogenes. The surface proteins (in blue) of Listeria enable us to view the bacteria. Actin, a constituent protein of cells, is shown in red and green.
Publication : Immunity

Colony-stimulating factor-1-dependent macrophages are responsible for IVIG protection in antibody-induced autoimmune disease

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Immunity - 01 Apr 2003

Bruhns P, Samuelsson A, Pollard JW, Ravetch JV

Link to Pubmed [PMID] – 12705859

Immunity 2003 Apr;18(4):573-81

The ability of IVIG to induce expression of Fc gamma RIIB 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 Fc gamma RIIB 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 Fc gamma RIIB on CSF-1-independent “effector” macrophages thereby raising the threshold required for Fc gamma RIII activation and preventing autoantibody-triggered inflammation.