ArticleThe American journal of pathology2000
Chemokine receptor 1 knockout abrogates natural killer cell recruitment and impairs type-1 cytokines in lymphoid tissue during pulmonary granuloma formation.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 48 citations in OpenAlex.
- Transcription factor MAFB controls type I and II interferon response-mediated host immunity inFrontiers in microbiology · 2022Article
- Differential Roles of Chemokines CCL2 and CCL7 in Monocytosis and Leukocyte Migration during West Nile Virus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Chemokines in innate and adaptive granuloma formation.Frontiers in immunology · 2013Article
- Chemokines and NK cells: regulators of development, trafficking and functions.Immunology letters · 2012Review
- Early viral replication in lymph nodes provides HIV with a means by which to escape NK-cell-mediated control.European journal of immunology · 2011Article
- Pulmonary fibrosis in response to environmental cues and molecular targets involved in its pathogenesis.Journal of toxicologic pathology · 2011Article
- Deficiency of chemokine receptor CCR1 causes osteopenia due to impaired functions of osteoclasts and osteoblasts.The Journal of biological chemistry · 2010Article
- Use of a T cell interferon gamma release assay in the investigation for suspected active tuberculosis in a low prevalence area.BMC infectious diseases · 2009Article
- A key role for CC chemokine receptor 1 in T-cell-mediated respiratory inflammation.The American journal of pathology · 2008Article
- Polymorphisms in chemokine receptor genes and susceptibility to Kawasaki disease.Clinical and experimental immunology · 2007Article
- Potential role of the chemokine macrophage inflammatory protein 1alpha in human and experimental schistosomiasis.Infection and immunity · 2005Article
- A proinflammatory chemokine, CCL3, sensitizes the heat- and capsaicin-gated ion channel TRPV1.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Impaired lung dendritic cell activation in CCR2 knockout mice.The American journal of pathology · 2004Article
- Mycobacterium tuberculosis in chemokine receptor 2-deficient mice: influence of dose on disease progression.Infection and immunity · 2002Article
- Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Mice with targeted mutation of chemokine receptor 1 (CCR1) were used to assess the contribution of CCR1 agonists to local, regional, and systemic inflammatory-related events during experimental pulmonary granuloma formation. Models of Th1 (type-1) and Th2 (type-2) cell-mediated lung granulomas were induced in wild-type (CCR+/+) and knockout (CCR1-/-) mice by embolizing Sepharose beads coupled to the purified protein derivative of Mycobacterium bovis or soluble antigens derived from Schistosoma mansoni eggs. Morphometric analysis indicated that granuloma sizes were unchanged in CCR1-/- mice, but flow cytometric analyses of dispersed granulomas revealed that natural killer cell recruitment to type-1 lesions was abrogated by 60%. Analysis of cytokine production by draining lymph node cultures showed altered expression in CCR1-/- mice characterized by reduced interleukin-2 and interferon-gamma in the type-1 response, and enhanced interleukin-5 and interleukin-13 in the type-2 response. Peripheral blood leukocytosis was also enhanced in the type-1 but not the type-2 response. These findings suggest that CCR1 agonists contribute to multiple immunoinflammatory events in the type-1 granulomatous response with natural killer cell accumulation being particularly sensitive to CCR1 disruption. Although functional efficacy of granulomas may be altered, chemokine redundancy and cytokine reserve seem to make the bulk of the exudative response resistant to CCR1 disruption.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.