IL-1β enhances inflammatory T H 2 differentiation

Caucheteux, Stephan M.; Hu‐Li, Jane; Guo, Liying; Bhattacharyya, Nisan; Crank, Michelle C.; Collins, Michael T.; Paul, William E.

doi:10.1016/j.jaci.2016.02.033

Cited by 31 publications

(26 citation statements)

References 10 publications

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“…40,41 At the moment, human studies with regard to anti-IL-33 are ongoing 42,43 and still have to prove their beneficial effect in asthmatic patients. As decreased IL-1β levels were observed in DEP+HDM-exposed mice that were prophylactically treated with r-sST2, but not therapeutically, this could be a potential mechanism of the observed discrepancy in inflammatory airway responses since IL-1β was previously found to be involved in type 2 promoting responses.…”

Section: Therapeutic R-sst2 Administration Does Not Modulate the Dementioning

confidence: 99%

“…As decreased IL-1β levels were observed in DEP+HDM-exposed mice that were prophylactically treated with r-sST2, but not therapeutically, this could be a potential mechanism of the observed discrepancy in inflammatory airway responses since IL-1β was previously found to be involved in type 2 promoting responses. 40,41 At the moment, human studies with regard to anti-IL-33 are ongoing 42,43 and still have to prove their beneficial effect in asthmatic patients. Moreover, it would be interesting to examine the functional role of other epithelial type 2-promoting cytokines, for example, IL-25…”

Section: Therapeutic R-sst2 Administration Does Not Modulate the Dementioning

confidence: 99%

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IL‐33 signalling contributes to pollutant‐induced allergic airway inflammation

Grove

Provoost

Braun

et al. 2018

Clin Experimental Allergy

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Section: Therapeutic R-sst2 Administration Does Not Modulate the Dementioning

confidence: 99%

Section: Therapeutic R-sst2 Administration Does Not Modulate the Dementioning

confidence: 99%

IL‐33 signalling contributes to pollutant‐induced allergic airway inflammation

Grove

Provoost

Braun

et al. 2018

Clin Experimental Allergy

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“…This Th2/Th17 phenotype is in line with the cytokines detected here. While IL-23 is obligatory for survival of Th17 cells 34 , IL-1β has been reported as an important factor of the Th2 immune response 35 . In the context of allergy, Dectin-signaling may therefore promote the present type 2-response while fueling the fungus-associated Th17 axis in parallel.…”

Section: Discussionmentioning

confidence: 99%

Human thioredoxin, a damage-associated molecular pattern and Malassezia-crossreactive autoallergen, modulates immune responses via the C-type lectin receptors Dectin-1 and Dectin-2

Roesner

Ernst

Chen

et al. 2019

Sci Rep

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Human thioredoxin (hTrx), which can be secreted from cells upon stress, functions in allergic skin inflammation as a T cell antigen due to homology and cross-reactivity with the fungal allergen Mala s13 of the skin-colonizing yeast Malassezia sympodialis . Recent studies have shown that cell wall polysaccharides of Malassezia are detected by the immune system via the C-type lectin receptors Dectin-1 and Dectin-2, which are expressed on myeloid cells. Therefore, this study aimed to investigate a putative interaction between Dectin-1, Dectin-2 and the allergens Mala s13 and hTrx. Stimulation of human monocyte-derived dendritic cells or macrophages with Mala s13 or hTrx resulted in remarkable secretion of IL-1β and IL-23. Blocking experiments suggest that hTrx induces IL-23 by Dectin-1 binding and IL-1β by binding to either Dectin-1 or Dectin-2. Regarding Mala s13, Dectin-1 appears to be involved in IL-1β signaling. Interference of Syk kinase function was performed to investigate downstream signaling, which led to diminished hTrx responses. In our experiments, we observed rapid internalization of Mala s13 and hTrx upon cell contact and we were able to confirm direct interaction with Dectin-1 as well as Dectin-2 applying a fusion protein screening platform. We hypothesize that this cytokine response may result in a Th2/Th17-polarizing milieu, which may play a key role during the allergic sensitization in the skin, where allergen presentation to T cells is accompanied by microbial colonization and skin inflammation.

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“…Regarding the "reverse mechanism", soluble inflammatory cytokines released into the TME by tumor-infiltrating immune cells could modulate CSC activities as well. For instance, the soluble factor IL-1 promoted Th-1 to Th-2 differentiation, thus contributing to the inhibition of antitumor immunity [67,68]. In particular, IL-1β stimulated the expression of the CSC-related marker ZEB1, induced resistance to chemotherapy, and increased sphere-forming efficiency in colon cancer cells, thus supporting a role for IL-1β in promoting CSC self-renewal and EMT [69].…”

Section: Immunomodulatory Molecules Stimulating Tumor Stemness: the Dmentioning

confidence: 94%

Cancer Stem Cells: Devil or Savior—Looking behind the Scenes of Immunotherapy Failure

Castagnoli

Santis

Volpari

et al. 2020

Cells

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Although the introduction of immunotherapy has tremendously improved the prognosis of patients with metastatic cancers of different histological origins, some tumors fail to respond or develop resistance. Broadening the clinical efficacy of currently available immunotherapy strategies requires an improved understanding of the biological mechanisms underlying cancer immune escape. Globally, tumor cells evade immune attack using two main strategies: avoiding recognition by immune cells and instigating an immunosuppressive tumor microenvironment. Emerging data suggest that the clinical efficacy of chemotherapy or molecularly targeted therapy is related to the ability of these therapies to target cancer stem cells (CSCs). However, little is known about the role of CSCs in mediating tumor resistance to immunotherapy. Due to their immunomodulating features and plasticity, CSCs can be especially proficient at evading immune surveillance, thus potentially representing the most prominent malignant cell component implicated in primary or acquired resistance to immunotherapy. The identification of immunomodulatory properties of CSCs that include mechanisms that regulate their interactions with immune cells, such as bidirectional release of particular cytokines/chemokines, fusion of CSCs with fusogenic stromal cells, and cell-to-cell communication exerted by extracellular vesicles, may significantly improve the efficacy of current immunotherapy strategies. The purpose of this review is to discuss the current scientific evidence linking CSC biological, immunological, and epigenetic features to tumor resistance to immunotherapy.

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IL-1β enhances inflammatory T H 2 differentiation

Cited by 31 publications

References 10 publications

IL‐33 signalling contributes to pollutant‐induced allergic airway inflammation

IL‐33 signalling contributes to pollutant‐induced allergic airway inflammation

Human thioredoxin, a damage-associated molecular pattern and Malassezia-crossreactive autoallergen, modulates immune responses via the C-type lectin receptors Dectin-1 and Dectin-2

Cancer Stem Cells: Devil or Savior—Looking behind the Scenes of Immunotherapy Failure

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