CD11c+ Cells Are Required for Antigen-Induced Increase of Mast Cells in the Lung

Dahlin, Joakim S.; Feinstein, Ricardo; Cui, Yue; Heyman, Birgitta; Hallgren, Jenny

doi:10.4049/jimmunol.1201200

Cited by 24 publications

(30 citation statements)

References 31 publications

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“…We have previously studied the mechanisms behind the massive recruitment of MCp to the lung, which occurs in an experimental asthma model in mice (8–12). The influx of MCp to the lung, which is dependent on VCAM-1 on the lung vascular endothelium and the expression of α4-integrins on the MCp (8), was followed by an increase in mature MCs in the lung (9, 12, 13).…”

Section: Introductionmentioning

confidence: 99%

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Influenza Infection in Mice Induces Accumulation of Lung Mast Cells through the Recruitment and Maturation of Mast Cell Progenitors

et al. 2017

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Mast cells (MCs) are powerful immune cells that mature in the peripheral tissues from bone marrow (BM)-derived mast cell progenitors (MCp). Accumulation of MCs in lung compartments where they are normally absent is thought to enhance symptoms in asthma. The enrichment of lung MCs is also observed in mice subjected to models of allergic airway inflammation. However, whether other types of lung inflammation trigger increased number of MCp, which give rise to MCs, is unknown. Here, mouse-adapted H1N1 influenza A was used as a model of respiratory virus infection. Intranasal administration of the virus induced expression of VCAM-1 on the lung vascular endothelium and an extensive increase in integrin β7hi lung MCp. Experiments were performed to distinguish whether the influenza-induced increase in the number of lung MCp was triggered mainly by recruitment or in situ cell proliferation. A similar proportion of lung MCp from influenza-infected and PBS control mice were found to be in a proliferative state. Furthermore, BM chimeric mice were used in which the possibility of influenza-induced in situ cell proliferation of host MCp was prevented. Influenza infection in the chimeric mice induced a similar number of lung MCp as in normal mice. These experiments demonstrated that recruitment of MCp to the lung is the major mechanism behind the influenza-induced increase in lung MCp. Fifteen days post-infection, the influenza infection had elicited an immature MC population expressing intermediate levels of integrin β7, which was absent in controls. At the same time point, an increased number of toluidine blue+ MCs was detected in the upper central airways. When the inflammation was resolved, the MCs that accumulated in the lung upon influenza infection were gradually lost. In summary, our study reveals that influenza infection induces a transient accumulation of lung MCs through the recruitment and maturation of MCp. We speculate that temporary augmented numbers of lung MCs are a cause behind virus-induced exacerbations of MC-related lung diseases such as asthma.

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Section: Introductionmentioning

confidence: 99%

“…The influx of MCp to the lung, which is dependent on VCAM-1 on the lung vascular endothelium and the expression of α4-integrins on the MCp (8), was followed by an increase in mature MCs in the lung (9, 12, 13). Interestingly, VCAM-1 transcripts in the lungs of mice are upregulated from 2 to 8 days after influenza infection (14).…”

Section: Introductionmentioning

confidence: 99%

Influenza Infection in Mice Induces Accumulation of Lung Mast Cells through the Recruitment and Maturation of Mast Cell Progenitors

et al. 2017

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“…14 In mice with experimental allergic asthma, mast cell progenitors are recruited to the lung 15 and give rise to increased numbers of lung mast cells. [16][17][18] In humans, mast cells can be derived from CD34…”

Section: Introductionmentioning

confidence: 99%

Lin− CD34hi CD117int/hi FcεRI+ cells in human blood constitute a rare population of mast cell progenitors

Dahlin¹,

Malinovschi²,

Öhrvik³

et al. 2016

Blood

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“…Cells were stained in FACS buffer (2% FCS in PBS, pH 7.4) after pre-incubation with anti-CD16/32. For intracellular staining of IL-4, re-stimulation of mononuclear cells was performed as described (17). …”

Section: Methodsmentioning

confidence: 99%

Mouse Mast Cell Protease-6 and MHC Are Involved in the Development of Experimental Asthma

Cui

Dahlin

Feinstein

et al. 2014

The Journal of Immunology

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Allergic asthma is a complex disease with a strong genetic component where mast cells play a major role by the release of pro-inflammatory mediators. In the mouse, mast cell protease-6 (mMCP-6) closely resembles the human version of mast cell tryptase, β-tryptase. The gene that encodes mMCP-6, Tpsb2, resides close by the H-2 complex (MHC gene) on chromosome 17. Thus, when the original mMCP-6 knockout mice were backcrossed to the BALB/c strain, these mice were carrying the 129/Sv haplotype of MHC (mMCP-6−/−/H-2bc). Further backcrossing yielded mMCP-6−/− mice with the BALB/c MHC locus. BALB/c mice were compared with mMCP-6−/− and mMCP-6−/−/H-2bc mice in a mouse model of experimental asthma. While OVA-sensitized and challenged wild type mice displayed a striking airway hyperresponsiveness (AHR), mMCP-6−/− mice had less AHR that was comparable to that of mMCP-6−/−/H-2bc mice, suggesting that mMCP-6 is required for a full-blown AHR. The mMCP-6−/−/H-2bc mice had strikingly reduced lung inflammation, IgE-responses and Th2 cell-responses upon sensitization and challenge, whereas the mMCP-6−/− mice responded similarly to the wild type mice but with a minor decrease in bronchoalveolar lavage (BAL) eosinophils. These findings suggest that inflammatory Th2-responses are highly dependent on the MHC-haplotype and that they can develop essentially independently of mMCP-6 while mMCP-6 plays a key role in the development of AHR.

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CD11c+ Cells Are Required for Antigen-Induced Increase of Mast Cells in the Lung

Cited by 24 publications

References 31 publications

Influenza Infection in Mice Induces Accumulation of Lung Mast Cells through the Recruitment and Maturation of Mast Cell Progenitors

Influenza Infection in Mice Induces Accumulation of Lung Mast Cells through the Recruitment and Maturation of Mast Cell Progenitors

Lin− CD34hi CD117int/hi FcεRI+ cells in human blood constitute a rare population of mast cell progenitors

Mouse Mast Cell Protease-6 and MHC Are Involved in the Development of Experimental Asthma

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