Systemic Administration of Antigen-Pulsed Dendritic Cells Induces Experimental Allergic Asthma in Mice upon Aerosol Antigen Rechallenge

Graffi, Sebastian; Dekan, Gerhard; Stingl, Georg; Epstein, Michelle M.

doi:10.1006/clim.2002.5190

Cited by 25 publications

(16 citation statements)

References 61 publications

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“…One such cell type is the dendritic cell. A number of studies have recently been published indicating that BM-derived dendritic cells are critical in the differentiation and activation of TH2 cells in the lung (51,52 (56). However, we did not detect any c-kit ϩ , IgER ϩ , mast cells in the spleen or lung of treated mice (data not shown).…”

Section: Figure 8 Ova Priming Enhances Expression Of Il-4r␣contrasting

confidence: 52%

Complex Role of the IL-4 Receptor α in a Murine Model of Airway Inflammation: Expression of the IL-4 Receptor α on Nonlymphoid Cells of Bone Marrow Origin Contributes to Severity of Inflammation

Kelly-Welch¹,

Melo

Smith

et al. 2004

The Journal of Immunology

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Recent studies have suggested the IL-4Rα expressed on lung epithelium is necessary for TH2-mediated goblet cell differentiation and mucus hypersecretion in a murine model of allergic lung disease. However, the IL-4Rα is expressed on numerous cell types that could contribute to the overall pathology and severity of asthma. The relative role of the receptor on these cells has not yet been conclusively delineated. To dissect the contribution of IL-4Rα in the development of pulmonary allergic responses, we generated murine radiation bone marrow (BM) chimeras. BM from IL-4Rα+ or IL-4Rα− mice was transferred into recipient mice that expressed or lacked IL-4Rα. In the absence of IL-4Rα in recipient mice, there was no goblet cell metaplasia or mucus hypersecretion in response to OVA, even in the presence of TH2 cells and substantial eosinophilic infiltration. More importantly, we found that expression of the IL-4Rα on a nonlymphoid, MHC class II+, BM-derived cell type contributes to the severity of inflammation and mucus production. These results suggest that IL-4 and IL-13 contribute to the development of allergic inflammation by stimulating a complex interaction between IL-4Rα+ cell types of both bone marrow and non-bone marrow origin.

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Section: Figure 8 Ova Priming Enhances Expression Of Il-4r␣contrasting

confidence: 52%

Complex Role of the IL-4 Receptor α in a Murine Model of Airway Inflammation: Expression of the IL-4 Receptor α on Nonlymphoid Cells of Bone Marrow Origin Contributes to Severity of Inflammation

Kelly-Welch¹,

Melo

Smith

et al. 2004

The Journal of Immunology

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“…At the same time, the difference in protection between CD8␣ ϩ and CD8␣ Ϫ subsets from infected mice may reflect their difference of potency in inducing protective responses. Notably, most of the previous studies examined bone marrow-derived or peripheral monocyte-derived DC, which were manipulated in in vitro culture conditions to generate different DC subsets (45,46). These subsets were further examined by performing coculture with T cells or adoptively transferred to recipients after pulsing with Ags (45).…”

Section: Discussionmentioning

confidence: 99%

“…These subsets were further examined by performing coculture with T cells or adoptively transferred to recipients after pulsing with Ags (45). A few studies used splenic CD8␣ ϩ and CD8␣ Ϫ DC subsets, in which the DC subsets were pulsed with Ags in vitro followed by adoptive transfer of the cells (46). Although these approaches are useful in testing the immunological function of various Ags, the handling of these Ags by DC subsets in vitro may not necessarily reflect the physiological process in vivo.…”

Section: Discussionmentioning

confidence: 99%

Adoptive Transfer of CD8α+ Dendritic Cells (DC) Isolated from Mice Infected with Chlamydia muridarum Are More Potent in Inducing Protective Immunity Than CD8α− DC

Bilenki

Wang

Yang

et al. 2006

The Journal of Immunology

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Chlamydial infections are serious public health concerns worldwide. In this study, we examined the role of dendritic cell (DC) subsets in inducing protective immunity against chlamydial infection using an adoptive transfer approach. We found that CD11c+CD8α+ (double-positive, DP) DC, compared with CD11c+CD8α− (single-positive, SP) DC isolated from infected mice, are more potent inducers of protective immunity. Specifically, mice pretreated with DPDC from infected mice, upon infection with Chlamydia trachomatis mouse pneumonitis (MoPn), experienced significantly less severe body weight loss and in vivo chlamydial growth. Analysis of MoPn-driven cytokine production by immune cells revealed that mice that were treated with DPDC produced significantly higher levels of Th1 (TNF-α, IFN-γ, and IL-12) but lower levels of Th2 (IL-4, IL-5, and IL-13)-related cytokines than the recipients of SPDC following infection challenge. Moreover, DPDC-treated mice displayed significantly higher levels of MoPn-specific IgG2a production and delayed-type hypersensitivity responses compared with SPDC-treated mice. Furthermore, DPDC isolated from infected mice produced higher amounts of IL-12 and IL-10 in vitro in comparison with SPDC. These data indicate that CD8α+ DC have a significantly higher capacity in inducing protective immunity compared with CD8α− DC, demonstrating the crucial role of DC1-like cells in eliciting protection against C. trachomatis infection

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“…Recent studies showed that adoptively transferred DC pulsed with nonviable chlamydial organisms induced Chlamydia-specific Th1 immune responses, which were equally protective as live chlamydial immunization [24]. On the other hand, adoptive transfer of allergen-pulsed DC induced Th2-type immune responses and asthma-like reaction in mice [25].…”

Section: Introductionmentioning

confidence: 99%

Dendritic cells from Chlamydia‐infected mice show altered Toll‐like receptor expression and play a crucial role in inhibition of allergic responses to ovalbumin

et al. 2004

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Our previous study has shown that Chlamydia lung infection can inhibit local eosinophilic inflammation induced by allergen sensitization and challenge, which is correlated with altered cytokine production. In the present study, we examined the role played by dendritic cells (DC) in chlamydial infection-mediated modulation of allergic responses. The results showed that DC freshly isolated from Chlamydia-infected mice (iIDC), unlike those from naive control mice (iNDC), could efficiently modulate immune responses to ovalbumin in vitro and in vivo. Co-culture of freshly isolated DC with naive CD4 cells from T cell receptor transgenic mice (DO11.10) showed that iIDC directed Th1-dominant, while iNDC directed Th2-dominant, allergen-specific CD4 T cell responses. Moreover, adoptive transfer of iIDC, but not iNDC, could inhibit systemic and local eosinophilia induced by allergen exposure. The reduction of eosinophilia was associated with a decrease in IL-5 receptor expression on bone marrow cells and the production of IL-5 and IL-13 by T lymphocytes. Analysis of the DC showed that iIDC expressed significantly higher levels of mRNA for Toll-like receptor 9 and produced more IL-12 compared to iNDC. The data demonstrate a critical role played by DC in infection-mediated inhibition of allergic responses.

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Systemic Administration of Antigen-Pulsed Dendritic Cells Induces Experimental Allergic Asthma in Mice upon Aerosol Antigen Rechallenge

Cited by 25 publications

References 61 publications

Complex Role of the IL-4 Receptor α in a Murine Model of Airway Inflammation: Expression of the IL-4 Receptor α on Nonlymphoid Cells of Bone Marrow Origin Contributes to Severity of Inflammation

Complex Role of the IL-4 Receptor α in a Murine Model of Airway Inflammation: Expression of the IL-4 Receptor α on Nonlymphoid Cells of Bone Marrow Origin Contributes to Severity of Inflammation

Adoptive Transfer of CD8α+ Dendritic Cells (DC) Isolated from Mice Infected with Chlamydia muridarum Are More Potent in Inducing Protective Immunity Than CD8α− DC

Dendritic cells from Chlamydia‐infected mice show altered Toll‐like receptor expression and play a crucial role in inhibition of allergic responses to ovalbumin

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