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  • 1
    Online Resource
    Online Resource
    Allergic Inflammatory Response to Short Ragweed Allergenic Extract in HLA-DQ Transgenic Mice Lacking CD4 Gene
    The American Association of Immunologists ; 2002
    In:  The Journal of Immunology Vol. 168, No. 2 ( 2002-01-15), p. 890-899
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 168, No. 2 ( 2002-01-15), p. 890-899
    Abstract: To investigate the role of HLA-DQ molecules and/or CD4+ T cells in the pathogenesis of allergic asthma, we generated HLA-DQ6 and HLA-DQ8 transgenic mice lacking endogenous class II (Aβnull) and CD4 genes and challenged them intranasally with short ragweed allergenic extract (SRW). We found that DQ6/CD4null mice developed a strong eosinophilic infiltration into the bronchoalveolar lavage and lung tissue, while DQ8/CD4null mice were normal. However, neither cytokines nor eosinophil peroxidase in the bronchoalveolar lavage of DQ6/CD4null mice was found. In addition, the airway reactivity to methacholine was elevated moderately in DQ6/CD4null mice compared with the high response in DQ/CD4+ counterparts and was only partially augmented by CD4+ T cell transfer. The DQ6/CD4null mice showed Th1/Th2-type cytokines and SRW-specific Abs in the immune sera in contrast to a direct Th2 response observed in DQ6/CD4+ mice. The proliferative response of spleen mononuclear cells and peribronchial lymph node cells demonstrated that the response to SRW in DQ6/CD4null mice was mediated by HLA-DQ-restricted CD4−CD8−NK1.1− T cells. FACS analysis of PBMC and spleen mononuclear cells demonstrated an expansion of double-negative (DN) CD4−CD8−TCRαβ+ T cells in SRW-treated DQ6/CD4null mice. These cells produced IL-4, IL-5, IL-13, and IFN-γ when stimulated with immobilized anti-CD3. IL-5 ELISPOT assay revealed that DN T cells were the cellular origin of IL-5 in allergen-challenged DQ6/CD4null mice. Our study shows a role for HLA-DQ-restricted CD4+ and DN T cells in the allergic response.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.168.2.890
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2002
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    Semaphorins 4A and 4D in chronic inflammatory diseases
    Springer Science and Business Media LLC ; 2017
    In:  Inflammation Research Vol. 66, No. 2 ( 2017-2), p. 111-117
    Details
    In: Inflammation Research, Springer Science and Business Media LLC, Vol. 66, No. 2 ( 2017-2), p. 111-117
    Type of Medium: Online Resource
    ISSN: 1023-3830 , 1420-908X
    URL: Article
    DOI: 10.1007/s00011-016-0983-5
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 1459194-7
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  • 3
    Online Resource
    Online Resource
    STAT6 Controls the Number of Regulatory T Cells In Vivo, Thereby Regulating Allergic Lung Inflammation
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 191, No. 4 ( 2013-08-15), p. 1517-1528
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 191, No. 4 ( 2013-08-15), p. 1517-1528
    Abstract: STAT6 plays a central role in IL-4–mediated allergic responses. Several studies indicate that regulatory T cells (Tregs) can be modulated by IL-4 in vitro. We previously showed that STAT6−/− mice are highly resistant to allergic lung inflammation even when wild-type Th2 effectors were provided and that they have increased numbers of Tregs. However, the role of STAT6 in modulating Tregs in vivo during allergic lung inflammation has not been thoroughly investigated. To examine Treg and STAT6 interaction during allergic inflammation, STAT6−/−, STAT6xRAG2−/−, and RAG2−/− mice were subjected to OVA sensitization and challenge following adoptive transfer of OVA-specific, wild-type Th2 effectors with or without prior Treg depletion/inactivation, using anti-CD25 (PC61). As expected, STAT6−/− mice were highly resistant to airway inflammation and remodeling. In contrast, allergic lung inflammation was partially restored in STAT6−/− mice treated with PC61 to levels observed in STAT6xRAG2−/− mice. In some cases, STAT6xRAG2−/− mice were also given natural Tregs along with Th2 effectors. Adoptive transfer of natural Tregs caused a substantial reduction in bronchoalveolar lavage eosinophil composition and suppressed airway remodeling and T cell migration into the lung in STAT6xRAG2−/− mice to levels comparable to those in STAT6−/− mice. These results demonstrate the STAT6-dependent suppression of Tregs in vivo to promote allergic airway inflammation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1300486
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2013
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
    Online Resource
    Design, production and immunomodulatory potency of a novel allergen bioparticle
    Public Library of Science (PLoS) ; 2020
    In:  PLOS ONE Vol. 15, No. 12 ( 2020-12-1), p. e0242867-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 15, No. 12 ( 2020-12-1), p. e0242867-
    Abstract: Allergen immunotherapy (AIT) is the only disease-modifying treatment with evidence for sustained efficacy. However, it is poorly developed compared to symptomatic drugs. The main reasons come from treatment duration implying monthly injections during 3 to 5 years or daily sublingual use, and the risk of allergic side-effects. To become a more attractive alternative to lifelong symptomatic drug use, improvements to AIT are needed. Among the most promising new immunotherapy strategies is the use of bioparticles for the presentation of target antigen to the immune system as they can elicit strong T cell and B cell immune responses. Virus-like particles (VLPs) are a specific class of bioparticles in which the structural and immunogenic constituents are from viral origin. However, VLPs are ill-suited for use in AIT as their antigenicity is linked to structure. Recently, synthetic biology has been used to produce artificial modular bioparticles, in which supramolecular assemblies are made of elements from heterogeneous biological sources promoting the design and use of in vivo-assembling enveloped bioparticles for viral and non-viral antigens presentation. We have used a coiled-coil hybrid assembly for the design of an enveloped bioparticle (eBP) that present trimers of the Der p 2 allergen at its surface, This bioparticle was produced as recombinant and in vivo assembled eBPs in plant. This allergen biotherapeutic was used to demonstrate i) the capacity of plants to produce synthetic supramolecular allergen bioparticles, and ii) the immunomodulatory potential of naturally-assembled allergen bioparticles. Our results show that allergens exposed on eBPs induced a very strong IgG response consisting predominantly of IgG2a in favor of the TH1 response. Finally, our results demonstrate that rDer p 2 present on the surface of BPs show a very limited potential to stimulate the basophil degranulation of patient allergic to this allergen which is predictive of a high safety potential.
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
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    DOI: 10.1371/journal.pone.0242867
    DOI: 10.1371/journal.pone.0242867.g001
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    DOI: 10.1371/journal.pone.0242867.s001
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2020
    detail.hit.zdb_id: 2267670-3
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  • 5
    Online Resource
    Online Resource
    STAT6 Expression in Multiple Cell Types Mediates the Cooperative Development of Allergic Airway Disease
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 4 ( 2011-02-15), p. 2571-2583
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 4 ( 2011-02-15), p. 2571-2583
    Abstract: Th2 cells induce asthma through the secretion of cytokines. Two such cytokines, IL-4 and IL-13, are critical mediators of many features of this disease. They both share a common receptor subunit, IL-4Rα, and signal through the STAT6 pathway. STAT6−/− mice have impaired Th2 differentiation and reduced airway response to allergen. Transferred Th2 cells were not able to elicit eosinophilia in response to OVA in STAT6−/− mice. To clarify the role of STAT6 in allergic airway inflammation, we generated mouse bone marrow (BM) chimeras. We observed little to no eosinophilia in OVA-treated STAT6−/− mice even when STAT6+/+ BM or Th2 cells were provided. However, when Th2 cells were transferred to STAT6×Rag2−/− mice, we observed an eosinophilic response to OVA. Nevertheless, the expression of STAT6 on either BM-derived cells or lung resident cells enhanced the severity of OVA-induced eosinophilia. Moreover, when both the BM donor and recipient lacked lymphocytes, transferred Th2 cells were sufficient to induce the level of eosinophilia comparable with that of wild-type (WT) mice. The expression of STAT6 in BM-derived cells was more critical for the enhanced eosinophilic response. Furthermore, we found a significantly higher number of CD4+CD25+Foxp3+ T cells (regulatory T cells [Tregs]) in PBS- and OVA-treated STAT6−/− mouse lungs compared with that in WT animals suggesting that STAT6 limits both naturally occurring and Ag-induced Tregs. Tregs obtained from either WT or STAT6−/− mice were equally efficient in suppressing CD4+ T cell proliferation in vitro. Taken together, our studies demonstrate multiple STAT6-dependent and -independent features of allergic inflammation, which may impact treatments targeting STAT6.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1002567
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Cytokines in chronic respiratory diseases
    H1 Connect ; 2013
    In:  F1000 Biology Reports Vol. 5 ( 2013-2-1)
    Details
    In: F1000 Biology Reports, H1 Connect, Vol. 5 ( 2013-2-1)
    Type of Medium: Online Resource
    ISSN: 1757-594X
    URL: Journal
    URL: Article
    DOI: 10.3410/B
    DOI: 10.3410/B5-3
    Language: Unknown
    Publisher: H1 Connect
    Publication Date: 2013
    detail.hit.zdb_id: 2893099-X
    detail.hit.zdb_id: 2486077-3
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  • 7
    Online Resource
    Online Resource
    Expression of neuroimmune semaphorins 4A and 4D and their receptors in the lung is enhanced by allergen and vascular endothelial growth factor
    Springer Science and Business Media LLC ; 2011
    In:  BMC Immunology Vol. 12, No. 1 ( 2011-12)
    Details
    In: BMC Immunology, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2011-12)
    Abstract: Semaphorins were originally identified as molecules regulating a functional activity of axons in the nervous system. Sema4A and Sema4D were the first semaphorins found to be expressed on immune cells and were termed "immune semaphorins". It is known that Sema4A and Sema4D bind Tim-2 and CD72 expressed on leukocytes and PlexinD1 and B1 present on non-immune cells. These neuroimmune semaphorins and their receptors have been shown to play critical roles in many physiological and pathological processes including neuronal development, immune response regulation, cancer, autoimmune, cardiovascular, renal, and infectious diseases. However, the expression and regulation of Sema4A, Sema4D, and their receptors in normal and allergic lungs is undefined. Results Allergen treatment and lung-specific vascular endothelial growth factor (VEGF) expression induced asthma-like pathologies in the murine lungs. These experimental models of allergic airway inflammation were used for the expression analysis of immune semaphorins and their receptors employing immunohistochemistry and flow cytometry techniques. We found that besides accessory-like cells, Sema4A was also detected on bronchial epithelial and smooth muscle cells, whereas Sema4D expression was high on immune cells such as T and B lymphocytes. Surprisingly, under inflammation various cell types including macrophages, lymphocytes, and granulocytes in the lung expressed Tim-2, a previously defined marker for Th2 cells. CD72 was found on lung immune, inflammatory, and epithelial cells. Bronchial epithelial cells were positive for both plexins, whereas some endothelial cells selectively expressed Plexin D1. Plexin B1 expression was also detected on lung DC. Both allergen and VEGF upregulated the expression of neuroimmune semaphorins and their receptors in the lung tissue. However, the lung tissue Sema4A-Tim2 expression was rather weak, whereas Sema4D-CD72 ligand-receptor pair was vastly upregulated by allergen. Soluble Sema4D protein was present in the lung lysates and a whole Sema4A protein plus its dimer were readily detected in the bronchoalveolar (BAL) fluids under inflammation. Conclusions This study clearly shows that neuroimmune semaphorins Sema4A and Sema4D and their receptors might serve as potential markers for the allergic airway inflammatory diseases. Our current findings pave the way for further investigations of the role of immune semaphorins in inflammation and their use as potential therapeutic targets for the inflammatory lung conditions.
    Type of Medium: Online Resource
    ISSN: 1471-2172
    URL: Article
    DOI: 10.1186/1471-2172-12-30
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 2041500-X
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  • 8
    Online Resource
    Online Resource
    Transfer of in vivo primed transgenic T cells supports allergic lung inflammation and FIZZ1 and Ym1 production in an IL-4Rα and STAT6 dependent manner
    Springer Science and Business Media LLC ; 2011
    In:  BMC Immunology Vol. 12, No. 1 ( 2011-12)
    Details
    In: BMC Immunology, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2011-12)
    Abstract: CD4+ T helper type 2 (T H 2) cells, their cytokines IL-4, IL-5 and IL-13 and the transcription factor STAT6 are known to regulate various features of asthma including lung inflammation, mucus production and airway hyperreactivity and also drive alternative activation of macrophages (AAM). However, the precise roles played by the IL-4/IL-13 receptors and STAT6 in inducing AAM protein expression and modulating specific features of airway inflammation are still unclear. Since T H 2 differentiation and activation plays a pivotal role in this disease, we explored the possibility of developing an asthma model in mice using T cells that were differentiated in vivo . Results In this study, we monitored the activation and proliferation status of adoptively transferred allergen-specific naïve or in vivo primed CD4+ T cells. We found that both the naïve and in vivo primed T cells expressed similar levels of CD44 and IL-4. However, in vivo primed T cells underwent reduced proliferation in a lymphopenic environment when compared to naïve T cells. We then used these in vivo generated effector T cells in an asthma model. Although there was reduced inflammation in mice lacking IL-4Rα or STAT6, significant amounts of eosinophils were still present in the BAL and lung tissue. Moreover, specific AAM proteins YM1 and FIZZ1 were expressed by epithelial cells, while macrophages expressed only YM1 in RAG2 -/- mice. We further show that FIZZ1 and YM1 protein expression in the lung was completely dependent on signaling through the IL-4Rα and STAT6. Consistent with the enhanced inflammation and AAM protein expression, there was a significant increase in collagen deposition and smooth muscle thickening in RAG2 -/- mice compared to mice deficient in IL-4Rα or STAT6. Conclusions These results establish that transfer of in vivo primed CD4+ T cells can induce allergic lung inflammation. Furthermore, while IL-4/IL-13 signaling through IL-4Rα and STAT6 is essential for AAM protein expression, lung inflammation and eosinophilia are only partially dependent on this pathway. Further studies are required to identify other proteins and signaling pathways involved in airway inflammation.
    Type of Medium: Online Resource
    ISSN: 1471-2172
    URL: Article
    DOI: 10.1186/1471-2172-12-60
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 2041500-X
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  • 9
    Online Resource
    Online Resource
    156 Lung immune semaphorins and their receptors
    Elsevier BV ; 2008
    In:  Cytokine Vol. 43, No. 3 ( 2008-09), p. 272-273
    Details
    In: Cytokine, Elsevier BV, Vol. 43, No. 3 ( 2008-09), p. 272-273
    Type of Medium: Online Resource
    ISSN: 1043-4666
    URL: Article
    DOI: 10.1016/j.cyto.2008.07.199
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
    detail.hit.zdb_id: 1463198-2
    SSG: 12
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  • 10
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    Short ragweed allergen induces eosinophilic lung disease in HLA-DQ transgenic mice
    American Society for Clinical Investigation ; 1999
    In:  Journal of Clinical Investigation Vol. 103, No. 12 ( 1999-6-15), p. 1707-1717
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 103, No. 12 ( 1999-6-15), p. 1707-1717
    Type of Medium: Online Resource
    ISSN: 0021-9738
    URL: Article
    DOI: 10.1172/JCI6175
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 1999
    detail.hit.zdb_id: 2018375-6
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