Studies of macrophage function in murine systemic lupus erythematosus. 3. The nature, anatomical location, and reversibility of the phagocytic defect.
The defect in phagocytosis and binding of antibody-coated sheep erythrocytes (EA) by peritoneal macrophages of (NZB X NZW)F1 or B/W mice is not intrinsic, but is related to the development of the autoimmune disease process. The defect appears to be confined to peritoneal macrophages, since bone marrow (BM)-derived macrophages have normal to elevated activities in vitro. The peritoneal macrophage defect is not due to blockade of Fc receptors in vivo, as shown by long-term culture or recovery of phagocytic and binding activities after removal of Fc receptors by pronase, but represents a reduced number of receptors with slightly delayed turnover. The defect can be reversed by elicitation of activated macrophages with Corynebacterium parvum, thioglycollate, or proteose peptone in vivo. Normal Fc-mediated phagocytosis and binding by BM-derived macrophages cultured from untreated autoimmune mice is enhanced by pretreatment of mice with C. parvum, thioglycollate, or proteose peptone. The cause of the defect in Fc-mediated phagocytosis by resident peritoneal macrophages of autoimmune mice was not ascertained; it may be due to abnormal macrophage kinetics or to the local effects of lymphokines released as a result of other autoimmune changes.
Russell
P J
PJ
Cameron
F H
FH
D000818:Animals; D001853:Bone Marrow / Q000473:pathology; D002448:Cell Adhesion; D002478:Cells, Cultured; D007074:Immunoglobulin G; D008180:Lupus Erythematosus, Systemic / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D008264:Macrophages / Q000166:cytology / Q000276:immunology / Q000503:physiopathology*; D051379:Mice; D010587:Phagocytosis
D007074:Immunoglobulin G