B Cell–Intrinsic MyD88 Signaling Is Essential for IgE Responses in Lungs Exposed to Pollen Allergens

Matsushita, Kazunobu; Yoshimoto, Tomohiro

doi:10.4049/jimmunol.1401768

Cited by 23 publications

(23 citation statements)

References 61 publications

(107 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…or footpad immunization with OVA plus alum induces OVA-specific IgE responses independently of MyD88 (Schnare et al, 2001). However, a recent report demonstrates that the inhalation of OVA plus alum induces OVA-specific IgE responses that is totally dependent on MyD88 (Matsushita and Yoshimoto, 2014). Consistent with previous reports, the OVA-specific antibody concentrations were similar in WT and Myd88 À/À mice immunized i.p.…”

Section: Exposure Of Airways To Particulates Induces Unique Immune Resupporting

confidence: 88%

Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation

et al. 2016

View full text Add to dashboard Cite

Particulate pollution is thought to function as an adjuvant that can induce allergic responses. However, the exact cell types and immunological factors that initiate the lung-specific immune responses are unclear. We found that upon intratracheal instillation, particulates such as aluminum salts and silica killed alveolar macrophages (AMs), which then released interleukin-1α (IL-1α) and caused inducible bronchus-associated lymphoid tissue (iBALT) formation in the lung. IL-1α release continued for up to 2 weeks after particulate exposure, and type-2 allergic immune responses were induced by the inhalation of antigen during IL-1α release and iBALT formation, even long after particulate instillation. Recombinant IL-1α was sufficient to induce iBALTs, which coincided with subsequent immunoglobulin E responses, and IL-1-receptor-deficient mice failed to induce iBALT formation. Therefore, the AM-IL-1α-iBALT axis might be a therapeutic target for particulate-induced allergic inflammation.

show abstract

Section: Exposure Of Airways To Particulates Induces Unique Immune Resupporting

confidence: 88%

Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Thus, IL-33 is not required for the adjuvanticity of subcutaneously administered HP-β-CD. These findings were consistent with previous reports that alum induces a completely different response depending on its administration route (21,(25)(26)(27). Taken together, these results indicate that stimulation of the IL-33-dependent pathway is unique to the adjuvanticity of intranasally administered HP-β-CD.…”

Section: Intranasal Administration Of Hp-β-cd Has a Unique Mode Of Acsupporting

confidence: 93%

IL-33 Is Essential for Adjuvant Effect of Hydroxypropyl-β-Cyclodexrin on the Protective Intranasal Influenza Vaccination

et al. 2020

View full text Add to dashboard Cite

Vaccine adjuvants are traditionally used to augment and modulate the immunogenicity of vaccines, although in many cases it is unclear which specific molecules contribute to their stimulatory activity. We previously reported that both subcutaneous and intranasal administration of hydroxypropyl-β-cyclodextrin (HP-β-CD), a pharmaceutical excipient widely used to improve solubility, can act as an effective adjuvant for an influenza vaccine. However, the mechanisms by which mucosal immune pathway is critical for the intranasal adjuvant activity of HP-β-CD have not been fully delineated. Here, we show that intranasally administered HP-β-CD elicits a temporary release of IL-33 from alveolar epithelial type 2 cells in the lung; notably, IL-33 expression in these cells is not stimulated following the use of other vaccine adjuvants. The experiments using gene deficient mice suggested that IL-33/ST2 signaling is solely responsible for the adjuvant effect of HP-β-CD when it is administered intranasally. In contrast, the subcutaneous injection of HP-β-CD and the intranasal administration of alum, as a damage-associated molecular patterns (DAMPs)-inducing adjuvant, or cholera toxin, as a mucosal adjuvant, enhanced humoral immunity in an IL-33-independent manner, suggesting that the IL-33/ST2 pathway is unique to the adjuvanticity of intranasally administered HP-β-CD. Furthermore, the release of IL-33 was involved in the protective immunity against influenza virus infection which is induced by the intranasal administration of HP-β-CD-adjuvanted influenza split vaccine. In conclusion, our results suggest that an understanding of administration route-and tissue-specific immune responses is crucial for the design of unique vaccine adjuvants.

show abstract

“…injection of antigen with the adjuvant [47]. Interestingly, the proteins involved in IL-1 signaling, MyD88 and IL-1Rs, are dispensable for the effects of alum on antibody responses after ip or im injection [44,48,49] but are required for adjuvant effects of alum on IgE responses when instilled into the lung as a model particulate [50,51]. These effects are independent of the NALP3 inflammasome and appear to be related to the fact that alveolar macrophages undergo necrosis and thus release IL-1α [51] when exposed to alum whereas peritoneal macrophages do not.…”

Section: Insoluble Salts and Other Particulate Adjuvantsmentioning

confidence: 99%

Old and new adjuvants

McKee

Marrack

2017

Current Opinion in Immunology

172

122

View full text Add to dashboard Cite

B Cell–Intrinsic MyD88 Signaling Is Essential for IgE Responses in Lungs Exposed to Pollen Allergens

Cited by 23 publications

References 61 publications

Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation

Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation

IL-33 Is Essential for Adjuvant Effect of Hydroxypropyl-β-Cyclodexrin on the Protective Intranasal Influenza Vaccination

Old and new adjuvants

Contact Info

Product

Resources

About