Myeloid dendritic cells type 2 in allergic asthma

Allergy ◽  
2013 ◽  
Vol 68 (10) ◽  
pp. 1322-1326 ◽  
Author(s):  
B. Dua ◽  
S. Smith ◽  
T. Kinoshita ◽  
H. Imaoka ◽  
G. Gauvreau ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Allergic Asthma ◽  
Myeloid Dendritic Cells

Myeloid dendritic cells are primed in allergic asthma for thymic stromal lymphopoietin-mediated induction of Th2 and Th9 responses

Allergy ◽  
2014 ◽  
Vol 69 (8) ◽  
pp. 1068-1076 ◽  
Author(s):  
A. Froidure ◽  
C. Shen ◽  
D. Gras ◽  
J. Van Snick ◽  
P. Chanez ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Allergic Asthma ◽  
Thymic Stromal Lymphopoietin ◽  
Myeloid Dendritic Cells

scholarly journals Inhaled house dust programs pulmonary dendritic cells to promote type 2 T-cell responses by an indirect mechanism

2015 ◽  
Vol 309 (10) ◽  
pp. L1208-L1218 ◽  
Author(s):  
Timothy P. Moran ◽  
Keiko Nakano ◽  
Gregory S. Whitehead ◽  
Seddon Y. Thomas ◽  
Donald N. Cook ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Allergic Asthma ◽  
House Dust ◽  
Lavage Fluid ◽  
Th2 Cells ◽  
T Helper 2 ◽  
Cell Responses ◽  
Th2 Responses ◽  
Th2 Differentiation

The induction of allergen-specific T helper 2 (Th2) cells by lung dendritic cells (DCs) is a critical step in allergic asthma development. Airway delivery of purified allergens or microbial products can promote Th2 priming by lung DCs, but how environmentally relevant quantities and combinations of these factors affect lung DC function is unclear. Here, we investigated the ability of house dust extract (HDE), which contains a mixture of environmental adjuvants, to prime Th2 responses against an innocuous inhaled antigen. Inhalational exposure to HDE conditioned lung conventional DCs, but not monocyte-derived DCs, to induce antigen-specific Th2 differentiation. Conditioning of DCs by HDE was independent of Toll-like receptor 4 signaling, indicating that environmental endotoxin is dispensable for programming DCs to induce Th2 responses. DCs directly treated with HDE underwent maturation but were poor stimulators of Th2 differentiation. In contrast, DCs treated with bronchoalveolar lavage fluid (BALF) from HDE-exposed mice induced robust Th2 differentiation. DC conditioning by BALF was independent of the proallergic cytokines IL-25, IL-33, and thymic stromal lymphopoietin. BALF treatment of DCs resulted in upregulation of CD80 but low expression of CD40, CD86, and IL-12p40, which was associated with Th2 induction. These findings support a model whereby environmental adjuvants in house dust indirectly program DCs to prime Th2 responses by triggering the release of endogenous soluble factor(s) by airway cells. Identifying these factors could lead to novel therapeutic targets for allergic asthma.

scholarly journals Dendritic Cells: Critical Regulators of Allergic Asthma

2020 ◽  
Vol 21 (21) ◽  
pp. 7930 ◽  
Author(s):  
Ioannis Morianos ◽  
Maria Semitekolou
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Allergic Airway Inflammation ◽  
Chronic Inflammatory Disease ◽  
Antigen Presenting ◽  
Airborne Allergens

Allergic asthma is a chronic inflammatory disease of the airways characterized by airway hyperresponsiveness (AHR), chronic airway inflammation, and excessive T helper (Th) type 2 immune responses against harmless airborne allergens. Dendritic cells (DCs) represent the most potent antigen-presenting cells of the immune system that act as a bridge between innate and adaptive immunity. Pertinent to allergic asthma, distinct DC subsets are known to play a central role in initiating and maintaining allergen driven Th2 immune responses in the airways. Nevertheless, seminal studies have demonstrated that DCs can also restrain excessive asthmatic responses and thus contribute to the resolution of allergic airway inflammation and the maintenance of pulmonary tolerance. Notably, the transfer of tolerogenic DCs in vivo suppresses Th2 allergic responses and protects or even reverses established allergic airway inflammation. Thus, the identification of novel DC subsets that possess immunoregulatory properties and can efficiently control aberrant asthmatic responses is critical for the re-establishment of tolerance and the amelioration of the asthmatic disease phenotype.

scholarly journals Jagged1-expressing adenovirus-infected dendritic cells induce expansion of Foxp3+ regulatory T cells and alleviate T helper type 2-mediated allergic asthma in mice

Immunology ◽  
2018 ◽  
Vol 156 (2) ◽  
pp. 199-212 ◽  
Author(s):  
Chu-Lun Lin ◽  
Huei-Mei Huang ◽  
Chia-Ling Hsieh ◽  
Chia-Kwung Fan ◽  
Yueh-Lun Lee
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Regulatory T Cells ◽  
Allergic Asthma ◽  
T Helper ◽  
Helper Type

scholarly journals Fms-Like Tyrosine Kinase 3-Independent Dendritic Cells Are Major Mediators of Th2 Immune Responses in Allergen-Induced Asthmatic Mice

2020 ◽  
Vol 21 (24) ◽  
pp. 9508
Author(s):  
Sang Chul Park ◽  
Dahee Shim ◽  
Hongmin Kim ◽  
Yeeun Bak ◽  
Da Yeon Choi ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Tyrosine Kinase ◽  
Allergic Asthma ◽  
Lung Inflammation ◽  
In Vivo Models ◽  
Allergic Lung Inflammation ◽  
Th2 Responses

Dendritic cells (DCs) are the main mediators of Th2 immune responses in allergic asthma, and Fms-like tyrosine kinase 3 ligand (Flt3L) is an important growth factor for the development and homeostasis of DCs. This study identified the DC populations that primarily cause the initiation and development of allergic lung inflammation using Fms-like tyrosine kinase 3 (Flt3) knockout (KO) mice with allergen-induced allergic asthma. We observed type 2 allergic lung inflammation with goblet cell hyperplasia in Flt3 KO mice, despite a significant reduction in total DCs, particularly CD103+ DCs, which was barely detected. In addition, bone marrow-derived dendritic cells (BMDCs) from Flt3 KO mice directed Th2 immune responses in vitro, and the adoptive transfer of these BMDCs exacerbated allergic asthma with more marked Th2 responses than that of BMDCs from wild-type (WT) mice. Furthermore, we found that Flt3L regulated the in vitro expression of OX40 ligand (OX40L) in DCs, which is correlated with DC phenotype in in vivo models. In conclusion, we revealed that Flt3-independent CD11b+ DCs direct Th2 responses with the elevated OX40L and are the primary cause of allergic asthma. Our findings suggest that Flt3 is required to control type 2 allergic inflammation.

scholarly journals Streptococcus pneumoniae aminopeptidase N regulates dendritic cells that attenuates type‐2 airway inflammation in murine allergic asthma

2020 ◽  
Vol 177 (22) ◽  
pp. 5063-5077
Author(s):  
Guangying Wu ◽  
Xuemei Zhang ◽  
Xu Chen ◽  
Jian Wang ◽  
Jing Yang ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Streptococcus Pneumoniae ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Aminopeptidase N

Myeloid dendritic cells type 2 after allergen inhalation in asthmatic subjects

2014 ◽  
Vol 44 (7) ◽  
pp. 921-929 ◽  
Author(s):  
B. Dua ◽  
W. Tang ◽  
R. Watson ◽  
G. Gauvreau ◽  
P. M. O'Byrne
Keyword(s):  
Dendritic Cells ◽  
Myeloid Dendritic Cells ◽  
Allergen Inhalation

Human TSLP promotes CD40 ligand-induced IL-12 production by myeloid dendritic cells but maintains their Th2 priming potential

Blood ◽  
2005 ◽  
Vol 105 (12) ◽  
pp. 4749-4751 ◽  
Author(s):  
Norihiko Watanabe ◽  
Shino Hanabuchi ◽  
Marie-Annick Marloie-Provost ◽  
Svetlana Antonenko ◽  
Yong-Jun Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Late Phase ◽  
Cd40 Ligand ◽  
Interleukin 4 ◽  
Myeloid Dendritic Cells ◽  
Th2 Cytokine ◽  
Th2 Inflammation ◽  
Th1 And Th2 Cytokines

Abstract Interleukin-4 (IL-4), a major T-helper type 2 (Th2) cytokine, primes dendritic cells (DCs) for IL-12 production, suggesting a negative feedback loop to prevent dysregulated Th2 inflammation, such as allergy. We previously showed that human thymic stromal lymphopoietin (TSLP), highly expressed by keratinocytes of atopic dermatitis, activates CD11c+ DCs to induce the differentiation of naive CD4+ and CD8+ T cells into proallergic effectors. Here we show that TSLP primes DCs to produce large amounts of IL-12 after CD40 ligand stimulation, similar to IL-4 priming of DCs. In contrast to IL-4 priming, DCs activated with TSLP and CD40 ligand induce the differentiation of naive CD4+ T cells into effectors producing both Th1 and Th2 cytokines, a unique profile that is reminiscent of the late phase of allergy. Thus, TSLP is a major regulatory cytokine for IL-12 production by DCs, and TSLP-activated DCs could promote the persistence of Th2 inflammation even in the presence of IL-12-inducing signals. (Blood. 2005;105:4749-4751)

scholarly journals Irg1/itaconate metabolic pathway is a crucial determinant of dendritic cells immune-priming function and contributes to resolute allergen-induced airway inflammation

2021 ◽  
Author(s):  
Anil Kumar Jaiswal ◽  
Jyoti Yadav ◽  
Sangeet Makhija ◽  
Suman Mazumder ◽  
Amit Kumar Mitra ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Allergic Sensitization ◽  
Mucous Cell ◽  
Th2 Immune Response ◽  
Pulsed Dc

AbstractItaconate is produced from the mitochondrial TCA cycle enzyme aconitase decarboxylase (encoded by immune responsive gene1; Irg1) that exerts immunomodulatory function in myeloid cells. However, the role of the Irg1/itaconate pathway in dendritic cells (DC)-mediated airway inflammation and adaptive immunity to inhaled allergens, which are the primary antigen-presenting cells in allergic asthma, remains largely unknown. House dust mite (HDM)-challenged Irg1−/− mice displayed increases in eosinophilic airway inflammation, mucous cell metaplasia, and Th2 cytokine production with a mechanism involving impaired mite antigen presentations by DC. Adoptive transfer of HDM-pulsed DC from Irg1-deficient mice into naïve WT mice induced a similar phenotype of elevated type 2 airway inflammation and allergic sensitization. Untargeted metabolite analysis of HDM-pulsed DC revealed itaconate as one of the most abundant polar metabolites that potentially suppress mitochondrial oxidative damage. Furthermore, the immunomodulatory effect of itaconate was translated in vivo, where intranasal administration of 4-octyl itaconate 4-OI following antigen priming attenuated the manifestations of HDM-induced airway disease and Th2 immune response. Taken together, these data demonstrated for the first time a direct regulatory role of the Irg1/itaconate pathway in DC for the development of type 2 airway inflammation and suggest a possible therapeutic target in modulating allergic asthma.

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