T cell subsets, epitope mapping, and HLA-restriction in patients with allergic bronchopulmonary aspergillosis.

Chauhan, Bela; Knutsen, Alan P.; Hutcheson, Patricia S.; Slavin, Raymond G.; Bellone, Clifford J.

doi:10.1172/jci118675

Cited by 142 publications

(96 citation statements)

References 37 publications

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“…12,32,39 Other factors, such as HLA-DR/HLA-DQ subtypes and the presence of single nucleotide polymorphisms in the IL-4 binding site of IL-4 receptor alpha have also been described to associate with development of ABPA. [40][41][42] Longitudinal studies are needed to confirm that Af sensitization routinely precedes ABPA.…”

Section: Discussionmentioning

confidence: 99%

The basophil surface marker CD203c identifies Aspergillus species sensitization in patients with cystic fibrosis

Mirković

Lavelle

Azim

et al. 2016

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 99%

The basophil surface marker CD203c identifies Aspergillus species sensitization in patients with cystic fibrosis

Mirković

Lavelle

Azim

et al. 2016

Journal of Allergy and Clinical Immunology

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“…The underlying mechanism of the inflammatory response observed in allergic asthma is attributable primarily to the activities of CD4 1 T cells (1,44,45). Although several therapies are available for the treatment of asthma, they all have side effects or are ineffective in particular patients (46,47).…”

Section: Discussionmentioning

confidence: 99%

Airway Epithelial Indoleamine 2,3-Dioxygenase Inhibits CD4⁺T Cells duringAspergillus fumigatusAntigen Exposure

Paveglio¹,

Allard²,

Hodgkins³

et al. 2011

Am J Respir Cell Mol Biol

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Indoleamine 2,3-dioxygenase (IDO) suppresses the functions of CD4 1 T cells through its ability to metabolize the essential amino acid tryptophan. Although the activity of IDO is required for the immunosuppression of allergic airway disease by the Toll-LikeReceptor 9 (TLR9) agonist, oligonucleotides comprised of cytosine and guanine nucleotides linked by phosphodiester bonds (CpG) DNA, it is unclear whether IDO expression by resident lung epithelial cells is sufficient to elicit these effects. Therefore, we created a transgenic mouse inducibly overexpressing IDO within nonciliated airway epithelial cells. Upon inhalation of formalin-fixed Aspergillus fumigatus hyphal antigens, the overexpression of IDO from airway epithelial cells of these mice reduced the number of CD4 1 T cells within the inflamed lung and impaired the capacity of antigen-specific splenic CD4 1 effector T cells to secrete the cytokines IL-4, IL-5, IL-13, and IFN-g. Despite these effects, allergic airway disease pathology was largely unaffected in mice expressing IDO in airway epithelium. In support of the concept that dendritic cells are the major cell type contributing to the IDO-inducing effects of CpG DNA, mice expressing TLR9 only in the airway epithelium did not augment IDO expression subsequent to the administration of CpG DNA. Furthermore, the systemic depletion of CD11c 1 cells rendered mice incapable of CpG DNA-induced IDO expression. Our results demonstrate that an overexpression of IDO within the airway epithelium represents a novel mechanism by which the number of CD4 1 T cells recruited to the lung and their capacity to produce cytokines can be diminished in a model of allergic airway disease, and these results also highlight the critical role of dendritic cells in the antiasthmatic effects of IDO induction by CpG DNA.

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“…The requirement for MHC class II in the presentation assays was demonstrated using an anti-DR inhibition assay. For this assay, DR-blocking Ab (clone L243; BD PharMingen) was added at a concentration of 10 g/ml at the initiation of the hybridomas and APC cocultures (30). Presentation was allowed to occur for 24 h in culture, following which 100 l of supernatant was harvested and assayed for the presence of IL-2, as described above.…”

Section: Hybridoma Mbp Presentation and Dr Inhibition Assaysmentioning

confidence: 99%

Inducible Heat Shock Protein 70 Promotes Myelin Autoantigen Presentation by the HLA Class II

Mycko

Ćwiklińska

Szymański

et al. 2004

The Journal of Immunology

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In this study, we investigated the role of the inducible form of heat shock protein 70 (hsp70) in the presentation of the major putative autoantigen in multiple sclerosis, myelin basic protein (MBP), in the context of appropriate MHC class II. By coimmunoprecipitation, we found that MBP is associated with hsp70 in APC in an ATP/ADP-dependent manner. Additionally, using confocal microscopy, hsp70 was detected in the endocytic pathway of APC, where it colocalized with MBP and HLA-DR. The immunodominant epitopes of MBP 85–99 and 80–99 were shown to bind selectively and specifically to hsp70 by surface plasmon resonance. The functional significance of MBP interaction with hsp70 was demonstrated by the detection of enhanced responses of an MBP-specific T cell hybridoma to MBP and MBP 80–99 with increasing levels of hsp70 and reduced responses when hsp70 expression was diminished within APC-expressing DRA*0101, DRB1*1501 (DR1501). However, when MBP 85–99 was used as the stimulus, T cell hybridoma responses were not enhanced by hsp70 overexpression within APC, suggesting that hsp70 contributes to Ag processing rather than Ag presentation. The importance of a direct association between MBP and hsp70 in the presentation pathways was demonstrated by enhanced efficacy of MBP presentation by APC transfected with a plasmid vector encoding a fusion hsp70-MBP protein. This is the first report on the involvement of self-inducible hsp70 in MHC class II-dependent autoantigen processing by APC. It implicates that aberrant self hsp expression may lead to the enhancement/modulation of autoimmune responses.

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T cell subsets, epitope mapping, and HLA-restriction in patients with allergic bronchopulmonary aspergillosis.

Cited by 142 publications

References 37 publications

The basophil surface marker CD203c identifies Aspergillus species sensitization in patients with cystic fibrosis

The basophil surface marker CD203c identifies Aspergillus species sensitization in patients with cystic fibrosis

Airway Epithelial Indoleamine 2,3-Dioxygenase Inhibits CD4⁺T Cells duringAspergillus fumigatusAntigen Exposure

Inducible Heat Shock Protein 70 Promotes Myelin Autoantigen Presentation by the HLA Class II

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T cell subsets, epitope mapping, and HLA-restriction in patients with allergic bronchopulmonary aspergillosis.

Cited by 142 publications

References 37 publications

The basophil surface marker CD203c identifies Aspergillus species sensitization in patients with cystic fibrosis

The basophil surface marker CD203c identifies Aspergillus species sensitization in patients with cystic fibrosis

Airway Epithelial Indoleamine 2,3-Dioxygenase Inhibits CD4+T Cells duringAspergillus fumigatusAntigen Exposure

Inducible Heat Shock Protein 70 Promotes Myelin Autoantigen Presentation by the HLA Class II

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Airway Epithelial Indoleamine 2,3-Dioxygenase Inhibits CD4⁺T Cells duringAspergillus fumigatusAntigen Exposure