Abstract
Three macrophage functions were studied in MRL-Ipr mice with autoimmune lymphoproliferative disease: surface expression of I-region-associated (Ia) antigens, tumor cytotoxicity, and interleukin-1 (IL-1) production. MRL-Ipr mice had a significantly increased representation of Ia-positive macrophages in the peritoneal cavity, compared to all normal strains of mice. In order to study the basis of this increase, thymocytes or splenocytes from MRL-Ipr mice were transplanted intraperitoneally into normal mice. Three days later the recipient mice had peritoneal exudates rich in Ia-positive macrophages. The cells which induced this response were T cells which elaborated a lymphokine responsible for the recruitment of Ia-positive macrophages. In previous studies from our laboratory using normal mice, lymphokine was secreted only following the interaction of immune T cells with antigen. The resident macrophages of MRL-Ipr mice were activated and killed tumor cells if triggered by an interaction with bacterial products, even without the addition of lymphokines. Secretion of IL-1 was normal. Our results indicate that the diseased MRL-1pr mice are characterized by (i) activated T cells that spontaneously secrete macrophage stimulatory molecules; and (ii) activated macrophages that show both an increased expression of Ia and lymphokine-independent triggering of tumoricidal activity.
Original language | English (US) |
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Pages (from-to) | 213-222 |
Number of pages | 10 |
Journal | Clinical Immunology and Immunopathology |
Volume | 25 |
Issue number | 2 |
DOIs | |
State | Published - Nov 1982 |
ASJC Scopus subject areas
- Immunology and Allergy
- Pathology and Forensic Medicine
- Immunology