T cell independence of bleomycin-induced pulmonary fibrosis

Moné, Hélène; Lake-Bullock, V; Zhu, J. Jim; Huang, Hao; Cohen, Donald A.; Kaplan, Alan M.

doi:10.1002/jlb.65.2.187

Cited by 113 publications

(97 citation statements)

References 24 publications

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“…Although we also found decreased numbers of CD4 lymphocytes the role of lymphocytes in bleomycin-induced pulmonary fibrosis is controversial (42). SCID mice develop fibrosis in similar fashion to wild-type mice (42). Interestingly there are increased numbers of eosinophils in areas of developing fibrosis in SCID mice (42).…”

Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 66%

“…SCID mice develop fibrosis in similar fashion to wild-type mice (42). Interestingly there are increased numbers of eosinophils in areas of developing fibrosis in SCID mice (42). In contrast Schrier et al (43) demonstrated attenuation of fibrosis in T cell-deficient nude mice as compared with euthymic mice, although these findings were in contrast to an earlier study showing similar fibrosis in nude and euthymic mice (44).…”

Section: Discussionmentioning

confidence: 81%

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The Role of the Th2 CC Chemokine Ligand CCL17 in Pulmonary Fibrosis

Belperio

Murray

et al. 2004

The Journal of Immunology

161

132

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Increasing evidence suggests that the development of pulmonary fibrosis is a Th2-mediated process. We hypothesized that the CC chemokines that are associated with a Th2 profile (CCL17 and CCL22) have an important role in the development of pulmonary fibrosis. We measured CCL17 and CCL22 during the pathogenesis of bleomycin-induced pulmonary fibrosis. We found that both CCL17 and CCL22 were significantly elevated through day 20 as compared with control mice. Peak expression of CCL22 preceded the peak levels of CCL17, as measured by real-time quantitative PCR. CCR4 is the receptor for CCL17 and CCL22 therefore, to further characterize the role of CCL17 and CCL22, we measured CCR4 mRNA in lung tissue of bleomycin-treated mice by real-time quantitative PCR. CCR4 was significantly elevated in bleomycin-treated mice as compared with control mice. Immunolocalization demonstrated that CCR4 was expressed predominantly on macrophages. Neutralization of CCL17, but not CCL22, led to a reduction in pulmonary fibrosis. Immunolocalization of bleomycin-treated lung tissue and human idiopathic pulmonary fibrosis tissue specimens showed that epithelial cells expressed CCL17. These findings demonstrate a central role for Th2 chemokines and the macrophage in the pathogenesis of pulmonary fibrosis and are further support for the role of a Th2 phenotype in the pathogenesis of pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 81%

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The Role of the Th2 CC Chemokine Ligand CCL17 in Pulmonary Fibrosis

Belperio

Murray

et al. 2004

The Journal of Immunology

161

132

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“…Several studies have shown that IFN-␥ production is increased in bleomycin-induced pulmonary fibrosis, suggesting a pathogenetic role for IFN-␥. 38,42 By contrast, another report demonstrated anti-fibrotic effects of IFN-␥ on bleomycin-induced pulmonary fibrosis. 49 Interestingly, lack of L-selectin and/or ICAM-1 expression did not affect IFN-␥ production ( Figure 7).…”

Section: Discussionmentioning

confidence: 97%

“…40,41 In addition, other proinflammatory cytokines, including IL-1␤ and IL-6, are involved in pulmonary fibrosis. 38,39 The loss of both ICAM-1 and L-selectin expression resulted in significantly decreased production of TNF-␣, IL-1␤, and IL-6 compared with wild-type littermates (Figure 7). The ICAM-1 deficiency reduced the production of IL-6 but not TNF-␣ and IL-1␤, while the L-selectin deficiency diminished the production of TNF-␣ but not IL-6 and IL-1␤.…”

Section: Discussionmentioning

confidence: 99%