Neutrophils are required for both the sensitization and elicitation phase of contact hypersensitivity

Weber, Felix; Németh, Tamás; Csepregi, Janka Zsófia; Dudeck, Anne; Roers, Axel; Ózsvári, Béla; Oswald, Eva; Puskás, László G.; Jakob, Thilo; Mócsai, Attila; Martin, Stefan F.

doi:10.1084/jem.20130062

Cited by 159 publications

(171 citation statements)

References 28 publications

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“…In agreement with our findings, novel results of a recent study established the requirement of neutrophils for the development of sensitization during CHS 15 . The study also revealed that hapten 2,4,6-tri nitrochlorobenzene-induced sensitization subsequent to the CHS response was impaired in antibody (NIMP-R14)-mediated neutrophil-depleted mice due to suppression of IFN-γ production (derived from skin dLN cells) and DC migration to the dLN 15 .…”

Section: Discussionsupporting

confidence: 93%

“…The study also revealed that hapten 2,4,6-tri nitrochlorobenzene-induced sensitization subsequent to the CHS response was impaired in antibody (NIMP-R14)-mediated neutrophil-depleted mice due to suppression of IFN-γ production (derived from skin dLN cells) and DC migration to the dLN 15 . However, our findings indicate that DNFB-induced CHS in the neutrophil depletion caused by the 1A8 antibody did not abrogate IFN-γ production.…”

Section: Discussionmentioning

confidence: 89%

“…With respect to the role of neutrophils in CHS, neutrophils were known to be important for the elicitation phase in which neutrophil recruitment to the hapten-challenged site led to the infiltration of hapten-specific CD8 + T cells and development of a CHS response 13,14 . In contrast, a more recent study suggested the requirement of neutrophils for both the sensitization and elicitation phase of CHS 15 . However, it remains unclear exactly how neutrophils exert its effect on the development of CHS.…”

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confidence: 81%

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Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity

Moniaga

Hara‐Chikuma

2016

Journal of Dermatological Science

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1Aquaporin-9 (AQP9), a water/glycerol channel protein, is expressed in several immune cells including neutrophils; however, its role in immune response remains unknown. Here we show the involvement of AQP9 in hapten-induced contact hypersensitivity (CHS), as a murine model of skin allergic contact dermatitis, using AQP9 knockout (AQP9 −/− ) mice. First, the CHS response to hapten dinitrofluorobenzene (DNFB) was impaired in AQP9 −/− mice compared with wild-type (WT) mice. Adoptive transfer of sensitized AQP9 −/− draining lymph node (dLN) cells into WT recipients resulted in a reduced CHS response, indicating impaired sensitization in AQP9 −/− mice. Second, administration of WT neutrophils into AQP9 −/− mice during sensitization rescued the impaired CHS response. Neutrophil recruitment to dLNs upon hapten application was attenuated by AQP9 deficiency. Coincidentally, AQP9 −/− neutrophils showed a reduced CC-chemokine receptor 7 (CCR7) ligand-induced migration efficacy, which was attributed to the attenuated recruitment of neutrophils to dLNs. Furthermore, we found that neutrophil deficiency, observed in AQP9 −/− or neutrophildepleted mice, decreased IL-17A production by dLN cells, which might be responsible for T cell activation during a subsequent CHS response. Taken together, these findings suggest that AQP9 is required for the development of sensitization during cutaneous acquired immune responses via regulating neutrophil function.Allergic contact dermatitis (ACD) is one of the most prevalent skin diseases consisting of sensitization and elicitation phases 1,2 . Advanced studies of hapten-induced contact hypersensitivity (CHS) as a murine model of ACD have expanded our understanding of the mechanism of allergic reactions occurring in the skin, especially the specific roles of a variety of immune cells. During the sensitization phase, hapten-bearing cutaneous dendritic cells (DCs) migrate into skin draining lymph nodes (dLNs), where the presentation of antigens to naïve T cells and subsequent T cell priming occur. During the elicitation phase, re-exposure to cognate hapten results in the recruitment of antigen-specific T cells to the site of allergen challenge and T cell-mediated tissue damage 2 . Increasing evidence shows that several subsets of immune cells, including various types of T cells (Th1, Th17, regulatory, and natural killer), DCs (dermal DCs and Langerhans cells), and mast cells, work synergistically in the skin and its dLNs to exert antigen presentation and T cell activation during the development of sensitization in CHS [3][4][5][6][7] . Neutrophils have long been considered as the final effector cells of an acute inflammatory response. On the other hand, accumulating evidence has extended the function of neutrophils to include activation and regulation during innate and adaptive immune responses 8,9 . Several studies have focused on the

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 89%

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confidence: 81%

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Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity

Moniaga

Hara‐Chikuma

2016

Journal of Dermatological Science

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“…At the site of infection/inflammation, neutrophils use an armamentarium of effector functions, including phagocytosis, respiratory burst, degranulation and neutrophil extracellular trap (NET) formation to eliminate the invading microorganisms [6,7]. In addition, neutrophils also participate in the organization of the overall immune response [6][7][8][9]. Despite being short-lived, terminally differentiated cells with limited transcriptional activity, they can undergo stimulus-induced gene expression changes leading to chemokine and cytokine release into the extracellular space [6,10,11].…”

Section: Overview Of Feedback Amplification Of Neutrophil Functionmentioning

confidence: 99%

Feedback Amplification of Neutrophil Function

Németh

Mócsai

2016

Trends in Immunology

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“…Using one Kit-independent MC-deficient strain, Dudeck et al reported evidence that MCs amplify rather than limit CHS responses, and concluded that the exaggerated CHS reactions observed in Kit-mutant animals are not caused by the absence of MCs but instead reflect other effects of the KIT deficiency (7,13). By contrast, based on findings in both Kit-mutant and Kit-independent MC-deficient mice, Gimenez-Rivera et al recently reported that MCs can suppress skin inflammation in a new mouse model of chronic CHS (14).…”

Section: Introductionmentioning

confidence: 99%

Imaging protective mast cells in living mice during severe contact hypersensitivity

Reber¹,

Sibilano²,

Starkl³

et al. 2017

JCI Insight

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Neutrophils are required for both the sensitization and elicitation phase of contact hypersensitivity

Abstract: Weber et al. report that neutrophils are required for both the sensitization and elicitation phase of contact hypersensitivity. Their results identify a novel role for neutrophils in shaping the adaptive immune response.

Cited by 159 publications

References 28 publications

Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity

Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity

Feedback Amplification of Neutrophil Function

Imaging protective mast cells in living mice during severe contact hypersensitivity

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