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Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation
Published on: July 23, 2012
Effects of Dendritic Cell Subset Manipulation on Airway Allergy in a Mouse Model
Ryosuke Murakami1, Yohko Nakagawa, Masumi Shimizu
1Departments of Microbiology and Immunology, Nippon Medical School, Tokyo, Japan.
Insights
Manipulating dendritic cell subsets can treat allergic rhinitis. Activating DEC-205+ DCs reduces allergic symptoms and histamine release, offering a new therapeutic strategy for allergic diseases.
Area of Science:
- Immunology
- Allergy Research
- Dendritic Cell Biology
Background:
- Two distinct dendritic cell (DC) subsets, DEC-205+ and 33D1+, regulate immune responses, with DEC-205+ DCs promoting Th1 polarization and 33D1+ DCs promoting Th2 dominance.
- Th1 polarization can be induced by depleting 33D1+ DCs or activating DEC-205+ DCs.
Purpose of the Study:
- To investigate the therapeutic potential of manipulating DC subsets in a mouse model of allergic rhinitis (AR).
- To evaluate the effects of 33D1+ DC depletion and DEC-205+ DC activation on AR symptoms and immune responses in vivo.
Main Methods:
- Mice were induced with allergic rhinitis using ovalbumin (OVA) and alum, followed by intranasal OVA challenges.
- Experimental groups received either 33D1+ DC depletion or DEC-205+ DC activation.
- Allergic symptoms, lavage fluid cell counts, and serum antibody levels (OVA-specific IgG1, IgG2a, IgE) were assessed.
Main Results:
- Both 33D1+ DC depletion and DEC-205+ DC activation significantly reduced allergic symptom scores in AR mice.
- 33D1+ DC depletion decreased serum antibody levels and nasal lavage fluid cells, but not bronchoalveolar lavage fluid cells.
- DEC-205+ DC activation suppressed histamine release from mast cells, likely via IL-12 secretion, and reduced allergic symptoms.
Conclusions:
- Targeting innate DC subsets presents a novel therapeutic strategy for allergic diseases.
- Activation of DEC-205+ DCs in vivo can mitigate allergic responses by promoting Th1 dominance and reducing histamine release from mast cells.
Background:
Two major distinct subsets of dendritic cells (DCs) are arranged to regulate immune responses: DEC-205+ DCs drive Th1 polarization and 33D1+ DCs establish Th2 dominancy. Th1 polarization can be achieved either by depletion of 33D1+ DCs with a 33D1-specific monoclonal antibody (mAb) or by activation of DEC-205+ DCs via intraperitoneal injection of α-galactosylceramide (α-GalCer). We studied the effect of 33D1+ DC depletion or DEC-205+ DC activation in vivo using an established mouse model of allergic rhinitis (AR).
Methods:
Mice were injected intraperitoneally with OVA plus alum and challenged 4 times with daily intranasal administration of OVA. Immediately after the last challenge, allergic symptoms such as sneezing and nasal rubbing as well as the number of cells in the bronchoalveolar lavage fluid (BALF) and nasal lavage fluid (NALF) were counted. The levels of serum OVA-specific IgG1, IgG2a, and IgE were also determined by ELISA.
Results:
The allergic symptom scores were significantly decreased in 33D1+ DC-depleted or DEC-205+ DC-activated AR mice. The levels of OVA-specific IgG1, IgG2a, and IgE, and the number of NALF cells, but not BALF cells, were reduced in 33D1+ DC-depleted but not in DEC-205+ DC-activated AR mice. Moreover, the activated DEC-205+ DCs suppressed histamine release from IgE-sensitized mast cells, probably through IL-12 secretion.
Conclusions:
The manipulation of innate DC subsets may provide a new therapeutic strategy for controlling various allergic diseases by reducing histamine release from IgE-sensitized mast cells by driving the immune response towards Th1 dominancy via activation of DEC-205+ DCs in vivo.
