The colony-stimulating factors and collagen-induced arthritis: exacerbation of disease by M-CSF and G-CSF and requirement for endogenous M-CSF
| Autor: | I K, Campbell, M J, Rich, R J, Bischof, J A, Hamilton |
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| Rok vydání: | 2000 |
| Předmět: |
Male
Mice Inbred C3H Macrophage Colony-Stimulating Factor Macrophages Antibodies Monoclonal Immunity Innate Mice Mutant Strains Recombinant Proteins Autoimmune Diseases Rats Arthritis Rheumatoid Mice Inbred C57BL Disease Models Animal Mice Mice Inbred DBA Osteopetrosis Granulocyte Colony-Stimulating Factor Animals Cell Lineage Immunization Collagen Chickens Granulocytes Interleukin-1 |
| Zdroj: | Journal of leukocyte biology. 68(1) |
| ISSN: | 0741-5400 |
| Popis: | There is increasing evidence that the colony-stimulating factors (CSFs) may play a part in chronic inflammatory autoimmune diseases, such as rheumatoid arthritis (RA). We examined the involvement of macrophage CSF (M-CSF or CSF-1) and granulocyte CSF (G-CSF) in collagen-induced arthritis (CIA), a murine model of RA. Daily injections of M-CSF or G-CSF, 20-24 days postprimary immunization with type II collagen, exacerbated disease symptoms in suboptimally immunized DBA/1 mice. Support for the involvement of endogenous M-CSF in CIA was obtained by studies in which neutralizing monoclonal antibody reduced the severity of established CIA and also by studies showing the resistance of M-CSF-deficient op/op mice to CIA induction. These studies show that M-CSF and G-CSF can be proinflammatory in CIA and provide evidence that macrophage- and granulocyte-lineage cells can exacerbate CIA. Our results also show that M-CSF-dependent cells are essential for CIA development, suggesting M-CSF may be a suitable target for therapeutic intervention in RA. |
| Databáze: | OpenAIRE |
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