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The colony‐stimulating factors and collagen‐induced arthritis: exacerbation of disease by M‐CSF and G‐CSF and requirement for endogenous M‐CSF
Author(s) -
Campbell Ian K.,
Rich Melissa J.,
Bischof Robert J.,
Hamilton John A.
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.68.1.144
Subject(s) - immunology , granulocyte macrophage colony stimulating factor , arthritis , rheumatoid arthritis , macrophage colony stimulating factor , granulocyte colony stimulating factor , proinflammatory cytokine , exacerbation , granulocyte colony stimulating factor receptor , medicine , autoimmune disease , colony stimulating factor , endogeny , biology , cytokine , antibody , macrophage , inflammation , chemotherapy , haematopoiesis , in vitro , genetics , stem cell , biochemistry
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.