| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Journal of Pathology, Vol 149, 559-574, Copyright © 1996 by American Society for Investigative Pathology
REGULAR ARTICLES |
S Umeda, K Takahashi, LD Shultz, M Naito and K Takagi
Second Department of Pathology, Kumamoto University School of Medicine, Japan.
The development of macrophage populations in osteopetrosis (op) mutant mice defective in production of functional macrophage colony- stimulating factor (M-CSF) and the response of these cell populations to exogenous M-CSF were used to classify macrophages into four groups: 1) monocytes, monocyte-derived macrophages, and osteoclasts, 2) MOMA-1- positive macrophages, 3) ER-TR9-positive macrophages, and 4) immature tissue macrophages. Monocytes, monocyte-derived macrophages, osteoclasts in bone, microglia in brain, synovial A cells, and MOMA-1- or ER-TR9-positive macrophages were deficient in op/op mice. The former three populations expanded to normal levels in op/op mice after daily M- CSF administration, indicating that they are developed and differentiated due to the effect of M-CSF supplied humorally. In contrast, the other cells did not respond or very slightly responded to M-CSF, and their development seems due to either M-CSF produced in situ or expression of receptor for M-CSF. Macrophages present in tissues of the mutant mice were immature and appear to be regulated by either granulocyte/macrophage colony-stimulating factor and/or interleukin-3 produced in situ or receptor expression. Northern blot analysis revealed different expressions of GM-CSF and IL-3 mRNA in various tissues of the op/op mice. However, granulocyte/macrophage colony- stimulating factor and interleukin-3 in serum were not detected by enzyme-linked immunosorbent assay. The immature macrophages differentiated and matured into resident macrophages after M-CSF administration, and some of these cells proliferated in response to M- CSF.
This article has been cited by other articles:
 |
|
 |
|
  K. Nakano, Y. Okada, K. Saito, R. Tanikawa, N. Sawamukai, Y. Sasaguri, T. Kohro, Y. Wada, T. Kodama, and Y. Tanaka Rheumatoid synovial endothelial cells produce macrophage colony-stimulating factor leading to osteoclastogenesis in rheumatoid arthritis Rheumatology, April 1, 2007; 46(4): 597 - 603. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Li and I. Tabas The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis J. Leukoc. Biol., February 1, 2007; 81(2): 483 - 491. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Aichele, J. Zinke, L. Grode, R. A. Schwendener, S. H. E. Kaufmann, and P. Seiler Macrophages of the Splenic Marginal Zone Are Essential for Trapping of Blood-Borne Particulate Antigen but Dispensable for Induction of Specific T Cell Responses J. Immunol., August 1, 2003; 171(3): 1148 - 1155. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Umeda, W. G. Beamer, K. Takagi, M. Naito, S.-I. Hayashi, H. Yonemitsu, T. Yi, and L. D. Shultz Deficiency of SHP-1 Protein-Tyrosine Phosphatase Activity Results in Heightened Osteoclast Function and Decreased Bone Density Am. J. Pathol., July 1, 1999; 155(1): 223 - 233. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Y. Myint, K. Miyakawa, M. Naito, L. D Shultz, Y. Oike, K.-i. Yamamura, and K. Takahashi Granulocyte/Macrophage Colony-Stimulating Factor and Interleukin-3 Correct Osteopetrosis in Mice with Osteopetrosis Mutation Am. J. Pathol., February 1, 1999; 154(2): 553 - 566. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. S. Stocks, W. C. Wang, J. W. Thompson, M. C. Stocks II, and E. M. Horwitz Malignant Infantile Osteopetrosis: Otolaryngological Complications and Management Arch Otolaryngol Head Neck Surg, June 1, 1998; 124(6): 689 - 694. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
