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Development and Functional Characterization of Murine Tolerogenic Dendritic Cells

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Published on: May 18, 2018

Modulation of dendritic cell function by cowshed dust extract.

Leonid Gorelik¹, Marion Kauth, Kirsten Gehlhar

¹Department of Experimental Pneumology, Ruhr-University Bochum, Bochum, Germany.

Innate Immunity

|November 29, 2008

Summary

Cowshed dust extract (CDE) exposure reduces dendritic cell allergy-inducing capacity. Prolonged CDE exposure inhibits allergic immune responses, involving an IL-10 dependent mechanism.

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Area of Science:

Immunology
Allergy Research
Dendritic Cell Biology

Background:

Cowshed dust extract (CDE) inhalation previously demonstrated reduced airway reactivity and inflammation in allergic asthma models.
The precise mechanisms underlying CDE's allergy-protective effects require further elucidation.
Investigating CDE's impact on dendritic cell (DC) function is crucial for understanding immune modulation.

Purpose of the Study:

To analyze the effects of CDE on dendritic cell biology and their capacity to induce allergic immune responses.
To elucidate the underlying mechanisms of CDE-induced immune modulation in a mouse model.

Main Methods:

Dendritic cells were generated from murine bone marrow cells (BMDC) and stimulated with CDE.
CDE-treated BMDCs were used to sensitize mice via the airways.

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Analysis included assessment of allergic immune response priming, DC phenotype (CD86 expression), and cytokine production (IL-10, IL-12p70, TNF-alpha).

In vitro IL-10 blockade was performed to assess its role.

Main Results:

CDE treatment of BMDCs 2 days prior to allergen pulsing prevented allergic sensitization.
BMDCs stimulated with CDE simultaneously with allergen induced a full allergic response.
CDE-treated BMDCs, unable to induce allergy, displayed an activated phenotype with high CD86 expression.
These cells transiently produced high levels of IL-10, IL-12p70, and TNF-alpha.
Blocking IL-10 partially restored the allergy-inducing capacity of CDE-exposed DCs.

Conclusions:

Prolonged exposure to CDE diminishes the allergy-inducing capacity of dendritic cells.
An autocrine IL-10 dependent mechanism appears to be involved in the CDE-induced downregulation of DC function.
These findings provide insights into the immunomodulatory effects of CDE relevant to allergy prevention.