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Corticotropin-releasing Factor Changes the Phenotype and Function of Dendritic Cells in Mouse Mesenteric Lymph Nodes.

Meng L, Lu Z, Xiaoteng W, Yue H, Bin L, Lina M, Zhe C - J Neurogastroenterol Motil (2015)

Bottom Line: MLNDCs treated with CRF-R1 antagonist exhibited a phenotype characterized by a less activated state and reduced surface expression of MHC-II, and consequently showed reduced capacity to stimulate T cells.In contrast, treatment of MLNDCs with CRF-R2 antagonist yielded an opposite result.CRF can alter the phenotype and function of intestinal DCs through direct action on CRF-R1 and CRF-R2, and activation of the CRF-R1 and CRF-R2 pathways yields opposing outcomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

ABSTRACT

Background/aims: Dendritic cells (DCs) are a significant contributor to the pathology of numerous chronic inflammatory autoimmune disorders; however, the effects of Corticotropin-releasing factor (CRF) on intestinal DCs are poorly understood. In this study, we investigated the role of CRF in alterations of intestinal dendritic cell phenotype and function.

Methods: Mouse mesenteric lymph node dendritic cells (MLNDCs) were obtained using magnetic bead sorting. Surface expression of CRF receptor type 1 (CRF-R1) and CRF-R2 was determined by double-labeling immunofluorescence and quantitative polymerase chain reaction (qPCR) and MLNDCs were subsequently exposed to CRF in the presence or absence of CRF-R1 and CRF-R2 antagonists. Expression of surface molecules (MHC-I and MHC-II) and co-stimulatory molecules (CD80 and CD86) was determined by flow cytometric and western blot analyses, and the T cell stimulatory capacity of MLNDCs was evaluated by mixed lymphocyte reaction.

Results: Immunofluorescent staining and quatitative polymerase chain reaction indicated that both the CRF receptors (CRF-R1 and CRF-2) are expressed on the surface of MLNDCs. Exposure to CRF increased the expression of MHC-II on MLNDCs as well as their capacity to stimulate T cell proliferation. MLNDCs treated with CRF-R1 antagonist exhibited a phenotype characterized by a less activated state and reduced surface expression of MHC-II, and consequently showed reduced capacity to stimulate T cells. In contrast, treatment of MLNDCs with CRF-R2 antagonist yielded an opposite result.

Conclusions: CRF can alter the phenotype and function of intestinal DCs through direct action on CRF-R1 and CRF-R2, and activation of the CRF-R1 and CRF-R2 pathways yields opposing outcomes.

No MeSH data available.


Related in: MedlinePlus

The expression of surface molecules of mesenteric lymph node dendritic cells (MLNDCs). The result of flow cytometry shows high level of MHC-II was expressed on the surface of MLNDCs, whereas the expression of CD80, CD86, and MHC-I was low.
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f3-jnm-21-571: The expression of surface molecules of mesenteric lymph node dendritic cells (MLNDCs). The result of flow cytometry shows high level of MHC-II was expressed on the surface of MLNDCs, whereas the expression of CD80, CD86, and MHC-I was low.

Mentions: In order to examine the effect of CRF on expression of MLNDC surface molecules cells were exposed to CRF (10 nM) for 24 hours, and the expression of CD86, CD80, MHC-II, and MHC-I was determined by flow cytometry and western blot analyses. Incubation of MLNDCs with CRF (10 nM) enhanced the expression of MHC-II (P < 0.05); in contrast, the expression of CD80, CD86, and MHC-I was unchanged (Fig. 3). To confirm that this effect was mediated via CRF receptors, MLNDCs were pretreated for 30 minutes with the selective CRF-R1 antagonist antalarmin (10 nM) prior to incubation with CRF (10 nM). Results indicated decreased expression of MHC-II with antalarmin pretreatment compared to CRF alone (P < 0.05). Moreover, pretreatment of MLNDCs for 30 minutes with the selective CRF-R2 antagonist astressin 2B (10 nM) prior to incubation with CRF (10 nM) resulted in markedly increased expression of MHC-II compared to CRF treatment alone (P < 0.05) (Fig. 4).


Corticotropin-releasing Factor Changes the Phenotype and Function of Dendritic Cells in Mouse Mesenteric Lymph Nodes.

Meng L, Lu Z, Xiaoteng W, Yue H, Bin L, Lina M, Zhe C - J Neurogastroenterol Motil (2015)

The expression of surface molecules of mesenteric lymph node dendritic cells (MLNDCs). The result of flow cytometry shows high level of MHC-II was expressed on the surface of MLNDCs, whereas the expression of CD80, CD86, and MHC-I was low.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4622140&req=5

f3-jnm-21-571: The expression of surface molecules of mesenteric lymph node dendritic cells (MLNDCs). The result of flow cytometry shows high level of MHC-II was expressed on the surface of MLNDCs, whereas the expression of CD80, CD86, and MHC-I was low.
Mentions: In order to examine the effect of CRF on expression of MLNDC surface molecules cells were exposed to CRF (10 nM) for 24 hours, and the expression of CD86, CD80, MHC-II, and MHC-I was determined by flow cytometry and western blot analyses. Incubation of MLNDCs with CRF (10 nM) enhanced the expression of MHC-II (P < 0.05); in contrast, the expression of CD80, CD86, and MHC-I was unchanged (Fig. 3). To confirm that this effect was mediated via CRF receptors, MLNDCs were pretreated for 30 minutes with the selective CRF-R1 antagonist antalarmin (10 nM) prior to incubation with CRF (10 nM). Results indicated decreased expression of MHC-II with antalarmin pretreatment compared to CRF alone (P < 0.05). Moreover, pretreatment of MLNDCs for 30 minutes with the selective CRF-R2 antagonist astressin 2B (10 nM) prior to incubation with CRF (10 nM) resulted in markedly increased expression of MHC-II compared to CRF treatment alone (P < 0.05) (Fig. 4).

Bottom Line: MLNDCs treated with CRF-R1 antagonist exhibited a phenotype characterized by a less activated state and reduced surface expression of MHC-II, and consequently showed reduced capacity to stimulate T cells.In contrast, treatment of MLNDCs with CRF-R2 antagonist yielded an opposite result.CRF can alter the phenotype and function of intestinal DCs through direct action on CRF-R1 and CRF-R2, and activation of the CRF-R1 and CRF-R2 pathways yields opposing outcomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

ABSTRACT

Background/aims: Dendritic cells (DCs) are a significant contributor to the pathology of numerous chronic inflammatory autoimmune disorders; however, the effects of Corticotropin-releasing factor (CRF) on intestinal DCs are poorly understood. In this study, we investigated the role of CRF in alterations of intestinal dendritic cell phenotype and function.

Methods: Mouse mesenteric lymph node dendritic cells (MLNDCs) were obtained using magnetic bead sorting. Surface expression of CRF receptor type 1 (CRF-R1) and CRF-R2 was determined by double-labeling immunofluorescence and quantitative polymerase chain reaction (qPCR) and MLNDCs were subsequently exposed to CRF in the presence or absence of CRF-R1 and CRF-R2 antagonists. Expression of surface molecules (MHC-I and MHC-II) and co-stimulatory molecules (CD80 and CD86) was determined by flow cytometric and western blot analyses, and the T cell stimulatory capacity of MLNDCs was evaluated by mixed lymphocyte reaction.

Results: Immunofluorescent staining and quatitative polymerase chain reaction indicated that both the CRF receptors (CRF-R1 and CRF-2) are expressed on the surface of MLNDCs. Exposure to CRF increased the expression of MHC-II on MLNDCs as well as their capacity to stimulate T cell proliferation. MLNDCs treated with CRF-R1 antagonist exhibited a phenotype characterized by a less activated state and reduced surface expression of MHC-II, and consequently showed reduced capacity to stimulate T cells. In contrast, treatment of MLNDCs with CRF-R2 antagonist yielded an opposite result.

Conclusions: CRF can alter the phenotype and function of intestinal DCs through direct action on CRF-R1 and CRF-R2, and activation of the CRF-R1 and CRF-R2 pathways yields opposing outcomes.

No MeSH data available.


Related in: MedlinePlus