Induction of high-affinity IgE receptor on lung dendritic cells during viral infection leads to mucous cell metaplasia

Grayson, Mitchell H.; Cheung, Dorothy; Rohlfing, Michelle; Kitchens, Robert T.; Spiegel, Daniel E.; Tucker, Jennifer; Battaile, John T.; Alevy, Yael G.; Yan, Le; Agapov, Eugene; Kim, Edy Y.; Holtzman, Michael J.

doi:10.1083/jcb1793oia5

Cited by 51 publications

(109 citation statements)

References 29 publications

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“…All three papers used a depleting antibody against the high-affinity IgE receptor (MAR-1) expressed on mast cells and basophils, and concluded that in the absence of these cells, Th2 cell immunity failed to develop. However, in our experiments employing 10-color flow cytometry to simultaneously look at basophils and DCs, Fc3RI is also expressed on a subset of CD11c hi DCs after allergen exposure (unpublished observations) and others have reported this receptor similarly to be induced by virus infection on lung DCs (Grayson et al, 2007). Therefore, it is also possible that some of the effects of ''specific'' basophil depletion were affecting DC subsets.…”

Section: Figure 3 Early Innate Cytokine Responses That Promote Allermentioning

confidence: 74%

“…The presence of specific IgE bound to the high-affinity receptor for IgE (Fc3RI) on DCs can lead to a 1000-fold lowering of the threshold for allergen recognition and in this way IgE might sustain Th2 cell responses via effects on DCs, as observed in clinical studies in which serum IgE was neutralized with anti-IgE monoclonal antibodies (omalizumab) (Maurer et al, 1998). Although this mechanism has been mainly described in human DCs, demonstration of the Fc3RI receptor in lung DCs propose a similar mechanism in the mouse (Grayson et al, 2007).…”

Section: Function Of Lung Dcs In Effector Th2 Cell Responsesmentioning

confidence: 95%

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Biology of Lung Dendritic Cells at the Origin of Asthma

Lambrecht

Hammad²

2009

Immunity

325

320

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Dendritic cells (DCs) initiate and maintain adaptive T helper 2 (Th2) cell responses to inhaled allergens in asthma. Various functions like antigen uptake, migration to the draining LNs, and induction of tolerance and adaptive immunity are not equally shared by all subsets of DCs, adding considerable complexity to understanding the immunology of allergic sensitization. Whereas the epithelium was initially considered solely as a physical barrier, it is now seen as a central player in controlling the function of lung DCs through release of Th2 cell-promoting cytokines. Although DCs are sufficient and necessary for induction of Th2 cell responses to many antigens, some allergens might require antigen presentation by basophils. Clinically relevant allergens, as well as environmental and genetic risk factors for allergy and asthma, often interfere directly or indirectly with the innate immune functions of airway epithelial cells, basophils, and DCs. This review summarizes the recent progress on our understanding how DCs control Th2 cell immunity in the lung.

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Section: Figure 3 Early Innate Cytokine Responses That Promote Allermentioning

confidence: 74%

Section: Function Of Lung Dcs In Effector Th2 Cell Responsesmentioning

confidence: 95%

Biology of Lung Dendritic Cells at the Origin of Asthma

Lambrecht

Hammad²

2009

Immunity

325

320

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“…Second, FcεR1 is displayed at high levels on circulating monocytes during asthma exacerbations. Third, expression of this receptor is increased by type I interferons (Grayson et al, 2007), which are produced at high levels during virus infection. Thus, viruses might trigger asthma exacerbations by increasing FcεR1 on circulating monocytes and by promoting the recruitment of FcεR1-expressing monocytes and inflammatory DCs to the lung.…”

Section: Inflammatory Dcsmentioning

confidence: 99%

Pulmonary Dendritic Cells

Cook¹,

Nakano²

2015

Comparative Biology of the Normal Lung

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“…Mechanistically, there is evidence that a single RSV infection has the capacity to cause acute and chronic changes on the airway epithelium, produce cytokine precursors, impact dendritic cells that may mediate airway neural pathways, and cause lasting immunomodulatory changes consistent with the asthma phenotype [139][140][141]. Furthermore, the use of Palivizumab, a monoclonal antibody directed at RSV which significantly decreases the severity of RSV bronchiolitis in preterm infants [142,143], has been related to lower rates of asthma development in some studies.…”

Section: Infectionsmentioning

confidence: 99%