Temporal Production of CCL28 Corresponds to Eosinophil Accumulation and Airway Hyperreactivity in Allergic Airway Inflammation

John, Alison E.; Thomas, Molly S.; Berlin, Aaron A.; Lukacs, Nicholas W.

doi:10.1016/s0002-9440(10)62258-4

Cited by 56 publications

(58 citation statements)

References 30 publications

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“…CCL28 is a human chemokine that has been shown to be an important player in the development of allergic airway inflammation and asthma (21,31,32). In this study we provide additional evidence linking CCL28 to the development of chronic asthma pathology.…”

Section: Discussionmentioning

confidence: 54%

Structure-Function Analysis of CCL28 in the Development of Post-viral Asthma

Thomas

Buelow

Nevins

et al. 2015

Journal of Biological Chemistry

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Background: CCL28 is associated with the pathogenesis of acute post-viral asthma. Results: In the absence of viral infection, natively folded CCL28 can induce asthma pathology, whereas unfolded CCL28 cannot. Conclusion:The structure of CCL28 is critical for its role in asthma pathogenesis. Significance: Inhibition of CCL28 presents a novel therapeutic option for the prevention of post-viral asthma.

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Section: Discussionmentioning

confidence: 54%

Structure-Function Analysis of CCL28 in the Development of Post-viral Asthma

Thomas

Buelow

Nevins

et al. 2015

Journal of Biological Chemistry

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“…In addition, CrmB and CrmD also may promote virus replication during late stages of the disease characterized by generalized skin lesions in VaV, monkeypox virus, and EV. This possibility is supported by the finding that the chemokines recognized by CrmB and CrmD are implicated in mucosal and skin inflammatory responses, and their neutralization results in impaired leukocyte recruitment and suppression of inflammatory responses (33,37,38).…”

Section: Discussionmentioning

confidence: 89%

A chemokine-binding domain in the tumor necrosis factor receptor from variola (smallpox) virus

Alejo

Ruiz-Argüello

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

134

162

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Variola virus (VaV) is the causative agent of smallpox, one of the most devastating diseases encountered by man, that was eradicated in 1980. The deliberate release of VaV would have catastrophic consequences on global public health. However, the mechanisms that contribute to smallpox pathogenesis are poorly understood at the molecular level. The ability of viruses to evade the host defense mechanisms is an important determinant of viral pathogenesis. Here we show that the tumor necrosis factor receptor (TNFR) homologue CrmB encoded by VaV functions not only as a soluble decoy TNFR but also as a highly specific binding protein for several chemokines that mediate recruitment of immune cells to mucosal surfaces and the skin, sites of virus entry and viral replication at late stages of smallpox. CrmB binds chemokines through its C-terminal domain, which is unrelated to TNFRs, was named smallpox virus-encoded chemokine receptor (SECRET) domain and uncovers a family of poxvirus chemokine inhibitors. An active SECRET domain was found in another viral TNFR (CrmD) and three secreted proteins encoded by orthopoxviruses. These findings identify a previously undescribed chemokine-binding and inhibitory domain unrelated to host chemokine receptors and a mechanism of immune modulation in VaV that may influence smallpox pathogenesis.immune evasion ͉ viral pathogenesis ͉ cytokine receptor ͉ poxvirus ͉ inflammation

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“…27 This nonredundancy could also be relevant in mucosa, as a recent study has shown a marginal role, if any, for CCR6 in mediating pDC homing into inflamed lungs on RSV infection. 50 In this model, CCL28 might overcome the need for CCR6 for an efficient pDC recruitment as its expression was reported to be increased in both human and mouse lung inflammation during asthma 51 and viral bronchiolitis. 52 Furthermore, given (1) the role of CCR9 in controlling pDC migration to the intestinal mucosa under both steady-state and inflammatory conditions 41 and (2) the identification of a CCR9-expressing pDC subset that resides in peripheral lymphoid tissues, 41,53 we control the expression of CCR9 on human pDCs.…”

Section: Pdcs Expressing Ccr6 and Ccr10 Produce Ifn-␣ In Response To mentioning

confidence: 99%

CCR6/CCR10-mediated plasmacytoid dendritic cell recruitment to inflamed epithelia after instruction in lymphoid tissues

Sisirak

Vey

Vanbervliet

et al. 2011

Blood

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Absent in peripheral tissues during homeostasis, human plasmacytoid dendritic cells (pDCs) are described in inflamed skin or mucosa. Here, we report that, unlike blood pDCs, a subset of tonsil pDCs express functional CCR6 and CCR10, and their respective ligands CCL20 and CCL27are detected in inflamed epithelia contacting blood dendritic cell antigen 2 ؉ pDCs. Moreover, pDCs are recruited to imiquimod-treated skin tumors in WT but not CCR6-deficient mice, and competitive adoptive transfers reveal that CCR6-deficient pDCs are impaired in homing to inflamed skin tumors after intravenous transfer. On IL-3 culture, CCR6 and CCR10 expression is induced on human blood pDCs that become responsive to CCL20 and CCL27/ CCL28, respectively. Interestingly, unlike myeloid DC, blood pDCs initially upregulate CCR7 expression and CCL19 responsiveness on IL-3 ؎ CpG-B and then acquire functional CCR6 and CCR10. Finally, IL-3-differentiated CCR6 ؉ CCR10 ؉ pDCs secrete high levels of IFN-␣ in response to virus. Overall, we propose an unexpected pDCs migratory model that may best apply for mucosal-associated lymphoid tissues. After CCR7-mediated extravasation into lymphoid tissues draining inflamed epithelia, blood pDCs may be instructed to up-regulate CCR6 and/or CCR10 allowing their homing into inflamed epithelia (in mucosae or skin IntroductionPlasmacytoid dendritic cells (pDCs) play an important role in innate antiviral immunity by rapidly secreting abundant type I IFNs after exposure to various RNA or DNA viruses. 1 This unique ability is mediated through their selective expression of TLR7 and TLR9, 2 involved in pathogen sensing. After activation, pDCs differentiate into a distinct type of mature DCs directing T-cell responses with high flexibility. 1 Thus, pDCs play a critical role at the interface between innate and adaptive immunity.pDCs are commonly detected in peripheral blood and lymphoid organs. 1 Unlike myeloid DC (mDCs), they are absent from peripheral epithelial tissues under steady-state conditions, fail to migrate in response to inflammatory chemokines in vitro, and are constitutively recruited from the blood to the lymph nodes through high endothelial venule, a process involving CD62L, CCR7, ChemR23, and CXCR3/4. 3-10 On maturation, both DC subsets up-regulate CCR7 expression and respond to the lymph nodehoming chemokines CCL19 and CCL21, 5,7,8 allowing their recruitment in T-cell areas where they initiate adaptive immune responses. It was recently shown in mice that CCR7 plays an essential role for the homing of pDCs, regardless of their activation status, to lymph node under both steady-state and inflammatory conditions. 10However, pDCs also accumulate in inflamed epithelial tissues during noninfectious and infectious disorders 9,11-18 and participate in inflammatory chronic diseases, such as psoriasis and systemic lupus erythematosus. 14,19,20 Moreover, pDC leukemia/lymphoma is often associated with isolated cutaneous lesions because of skin accumulation of leukemic pDCs. 21 Inducible CXCR3 ligands (CXCL9/10/11...

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Temporal Production of CCL28 Corresponds to Eosinophil Accumulation and Airway Hyperreactivity in Allergic Airway Inflammation

Cited by 56 publications

References 30 publications

Structure-Function Analysis of CCL28 in the Development of Post-viral Asthma

Structure-Function Analysis of CCL28 in the Development of Post-viral Asthma

A chemokine-binding domain in the tumor necrosis factor receptor from variola (smallpox) virus

CCR6/CCR10-mediated plasmacytoid dendritic cell recruitment to inflamed epithelia after instruction in lymphoid tissues

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