Lack of Retinoic Acid Leads to Increased Langerin-Expressing Dendritic Cells in Gut-Associated Lymphoid Tissues

Chang, Shau‐Jin; Cha, Hye‐Ran; Chang, Jae‐Hoon; Ko, Hyun–Jeong; Yang, Hyungjun; Malissen, Bernard; Iwata, Makoto; Kweon, Mi‐Na

doi:10.1053/j.gastro.2009.11.006

Cited by 39 publications

(44 citation statements)

References 36 publications

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“…DCs, excluding langerin + DCs, in the MLN of VAD mice secrete more inflammatory cytokines such as TNF-a and IL-6 than those of control diet-fed mice, and stimulate CD4 + T cells to secrete IFN-g and IL-17 (28). In addition to TNF-a and IL-6, we also found hypersecretion of IFN-g by MLN DCs of VAD mice (Fig.…”

Section: Discussionsupporting

confidence: 56%

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IFN-γ Secreted by CD103+ Dendritic Cells Leads to IgG Generation in the Mesenteric Lymph Node in the Absence of Vitamin A

Chang

Cha

Chang

et al. 2011

The Journal of Immunology

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Although the induction mechanism of secretory IgA has been well studied, that of IgG in the mucosal compartments is not well understood. In this study, vitamin A deficiency was convincingly shown to be associated with increased IgG in serum and intestinal fluid. We found increased numbers of IgG-secreting B cells in the lamina propria of the small intestine and mesenteric lymph node (MLN) of vitamin A-deficient (VAD) mice. Of note, IFN-γ secreted by MLN dendritic cells (DCs) was significantly augmented in VAD mice, unlike control mice, and CD103+ DCs were the main subsets to secrete IFN-γ. The aberrant increase of IgG in VAD mice can be ascribable to IFN-γ, because IFN-γ−/− VAD mice have normal IgG levels and the addition of rIFN-γ increased IgG production by B cells cocultured with MLN DCs from IFN-γ−/− VAD mice. Oral feeding of antibiotics resulted in significant reduction of IgG in VAD mice, indicating a critical role for altered commensal bacteria for IgG class-switching recombination in the absence of vitamin A. Collectively, vitamin A deficiency provokes the generation of IFN-γ–secreting CD103+ DCs, which may be a critical regulator for IgG generation in the MLN.

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Section: Discussionsupporting

confidence: 56%

“…We previously showed that lack of vitamin A leads to reconstruction of DC subsets in GALT (28). DCs, excluding langerin + DCs, in the MLN of VAD mice secrete more inflammatory cytokines such as TNF-a and IL-6 than those of control diet-fed mice, and stimulate CD4 + T cells to secrete IFN-g and IL-17 (28).…”

Section: Discussionmentioning

confidence: 99%

IFN-γ Secreted by CD103+ Dendritic Cells Leads to IgG Generation in the Mesenteric Lymph Node in the Absence of Vitamin A

Chang

Cha

Chang

et al. 2011

The Journal of Immunology

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“…In addition to promoting RALDH activity, s.c. applied RA decreased the frequency of Langerin + DCs in skin-draining LNs. Similarly, Chang and colleagues suggest a link between availability of RA and expression of Langerin by showing that vitamin A-deficient mice display increased numbers of Langerin + DCs in GALT (29). It remains to be determined whether the reduction of Langerin + ingLN DCs is responsible for induction of a mucosal immune response after RA-supplemented s.c. immunization.…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid induces homing of protective T and B cells to the gut after subcutaneous immunization in mice

Hammerschmidt¹,

Friedrichsen²,

Boelter³

et al. 2011

J. Clin. Invest.

138

124

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“…It has been shown that VD 3 inhibits the expression of RALDH2 in mouse DCs (32). In addition, VD 3 represses RA-transcriptional activity via VDR in human myeloid cells (33).…”

Section: Discussionmentioning

confidence: 99%

Human CD1c+ Myeloid Dendritic Cells Acquire a High Level of Retinoic Acid–Producing Capacity in Response to Vitamin D3

Sato

Kitawaki

Fujita

et al. 2013

The Journal of Immunology

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All-trans-retinoic acid (RA) plays a critical role in maintaining immune homeostasis. Mouse intestinal CD103+ dendritic cells (DCs) produce a high level of RA by highly expressing retinal dehydrogenase (RALDH)2, an enzyme that converts retinal to RA, and induce gut-homing T cells. However, it has not been identified which subset of human DCs produce a high level of RA. In this study, we show that CD1c+ blood myeloid DCs (mDCs) but not CD141high mDCs or plasmacytoid DCs exhibited a high level of RALDH2 mRNA and aldehyde dehydrogenase (ALDH) activity in an RA- and p38-dependent manner when stimulated with 1α,25-dihydroxyvitamin D3 (VD3) in the presence of GM-CSF. The ALDH activity was abrogated by TLR ligands or TNF. CD103− rather than CD103+ human mesenteric lymph node mDCs gained ALDH activity in response to VD3. Furthermore, unlike in humans, mouse conventional DCs in the spleen and mesenteric lymph nodes gained ALDH activity in response to GM-CSF alone. RALDH2high CD1c+ mDCs stimulated naive CD4+ T cells to express gut-homing molecules and to produce Th2 cytokines in an RA-dependent manner. This study suggests that CD1c+ mDCs are a major human DC subset that produces RA in response to VD3 in the steady state. The “vitamin D – CD1c+ mDC – RA” axis may constitute an important immune component for maintaining tissue homeostasis in humans.

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Lack of Retinoic Acid Leads to Increased Langerin-Expressing Dendritic Cells in Gut-Associated Lymphoid Tissues

Cited by 39 publications

References 36 publications

IFN-γ Secreted by CD103+ Dendritic Cells Leads to IgG Generation in the Mesenteric Lymph Node in the Absence of Vitamin A

IFN-γ Secreted by CD103+ Dendritic Cells Leads to IgG Generation in the Mesenteric Lymph Node in the Absence of Vitamin A

Retinoic acid induces homing of protective T and B cells to the gut after subcutaneous immunization in mice

Human CD1c+ Myeloid Dendritic Cells Acquire a High Level of Retinoic Acid–Producing Capacity in Response to Vitamin D3

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