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A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection

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A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection. / Lundie, Rachel J; Webb, Lauren M; Marley, Angela K; Phythian-Adams, Alexander T; Cook, Peter C; Jackson-Jones, Lucy H; Brown, Sheila; Maizels, Rick M; Boon, Louis; O'Keeffe, Meredith; MacDonald, Andrew S.

In: Immunology and Cell Biology, Vol. 94, No. 4, 04.2016, p. 400-410.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Lundie, RJ, Webb, LM, Marley, AK, Phythian-Adams, AT, Cook, PC, Jackson-Jones, LH, Brown, S, Maizels, RM, Boon, L, O'Keeffe, M & MacDonald, AS 2016, 'A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection', Immunology and Cell Biology, vol. 94, no. 4, pp. 400-410. https://doi.org/10.1038/icb.2015.114

APA

Lundie, R. J., Webb, L. M., Marley, A. K., Phythian-Adams, A. T., Cook, P. C., Jackson-Jones, L. H., Brown, S., Maizels, R. M., Boon, L., O'Keeffe, M., & MacDonald, A. S. (2016). A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection. Immunology and Cell Biology, 94(4), 400-410. https://doi.org/10.1038/icb.2015.114

Vancouver

Lundie RJ, Webb LM, Marley AK, Phythian-Adams AT, Cook PC, Jackson-Jones LH et al. A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection. Immunology and Cell Biology. 2016 Apr;94(4):400-410. https://doi.org/10.1038/icb.2015.114

Author

Lundie, Rachel J ; Webb, Lauren M ; Marley, Angela K ; Phythian-Adams, Alexander T ; Cook, Peter C ; Jackson-Jones, Lucy H ; Brown, Sheila ; Maizels, Rick M ; Boon, Louis ; O'Keeffe, Meredith ; MacDonald, Andrew S. / A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection. In: Immunology and Cell Biology. 2016 ; Vol. 94, No. 4. pp. 400-410.

Bibtex

@article{2480eadfd6484e1d803a56bd4dc937f1,
title = "A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection",
abstract = "Dendritic cells (DCs) are the key initiators of T-helper (Th) 2 immune responses against the parasitic helminth Schistosoma mansoni. Although the liver is one of the main sites of antigen deposition during infection with this parasite, it is not yet clear how distinct DC subtypes in this tissue respond to S. mansoni antigens in vivo, or how the liver microenvironment might influence DC function during establishment of the Th2 response. In this study, we show that hepatic DC subsets undergo distinct activation processes in vivo following murine infection with S. mansoni. Conventional DCs (cDCs) from schistosome-infected mice upregulated expression of the costimulatory molecule CD40 and were capable of priming naive CD4(+) T cells, whereas plasmacytoid DCs (pDCs) upregulated expression of MHC class II, CD86 and CD40 but were unable to support the expansion of either naive or effector/memory CD4(+) T cells. Importantly, in vivo depletion of pDCs revealed that this subset was dispensable for either maintenance or regulation of the hepatic Th2 effector response during acute S. mansoni infection. Our data provides strong evidence that S. mansoni infection favors the establishment of an immunogenic, rather than tolerogenic, liver microenvironment that conditions cDCs to initiate and maintain Th2 immunity in the context of ongoing antigen exposure. ",
keywords = "Animals, Antigens, Helminth, Cell Differentiation, Cells, Cultured, Dendritic Cells, Liver, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Schistosoma mansoni, Schistosomiasis mansoni, Th2 Cells, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Lundie, {Rachel J} and Webb, {Lauren M} and Marley, {Angela K} and Phythian-Adams, {Alexander T} and Cook, {Peter C} and Jackson-Jones, {Lucy H} and Sheila Brown and Maizels, {Rick M} and Louis Boon and Meredith O'Keeffe and MacDonald, {Andrew S}",
year = "2016",
month = apr,
doi = "10.1038/icb.2015.114",
language = "English",
volume = "94",
pages = "400--410",
journal = "Immunology and Cell Biology",
number = "4",

}

RIS

TY - JOUR

T1 - A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection

AU - Lundie, Rachel J

AU - Webb, Lauren M

AU - Marley, Angela K

AU - Phythian-Adams, Alexander T

AU - Cook, Peter C

AU - Jackson-Jones, Lucy H

AU - Brown, Sheila

AU - Maizels, Rick M

AU - Boon, Louis

AU - O'Keeffe, Meredith

AU - MacDonald, Andrew S

PY - 2016/4

Y1 - 2016/4

N2 - Dendritic cells (DCs) are the key initiators of T-helper (Th) 2 immune responses against the parasitic helminth Schistosoma mansoni. Although the liver is one of the main sites of antigen deposition during infection with this parasite, it is not yet clear how distinct DC subtypes in this tissue respond to S. mansoni antigens in vivo, or how the liver microenvironment might influence DC function during establishment of the Th2 response. In this study, we show that hepatic DC subsets undergo distinct activation processes in vivo following murine infection with S. mansoni. Conventional DCs (cDCs) from schistosome-infected mice upregulated expression of the costimulatory molecule CD40 and were capable of priming naive CD4(+) T cells, whereas plasmacytoid DCs (pDCs) upregulated expression of MHC class II, CD86 and CD40 but were unable to support the expansion of either naive or effector/memory CD4(+) T cells. Importantly, in vivo depletion of pDCs revealed that this subset was dispensable for either maintenance or regulation of the hepatic Th2 effector response during acute S. mansoni infection. Our data provides strong evidence that S. mansoni infection favors the establishment of an immunogenic, rather than tolerogenic, liver microenvironment that conditions cDCs to initiate and maintain Th2 immunity in the context of ongoing antigen exposure.

AB - Dendritic cells (DCs) are the key initiators of T-helper (Th) 2 immune responses against the parasitic helminth Schistosoma mansoni. Although the liver is one of the main sites of antigen deposition during infection with this parasite, it is not yet clear how distinct DC subtypes in this tissue respond to S. mansoni antigens in vivo, or how the liver microenvironment might influence DC function during establishment of the Th2 response. In this study, we show that hepatic DC subsets undergo distinct activation processes in vivo following murine infection with S. mansoni. Conventional DCs (cDCs) from schistosome-infected mice upregulated expression of the costimulatory molecule CD40 and were capable of priming naive CD4(+) T cells, whereas plasmacytoid DCs (pDCs) upregulated expression of MHC class II, CD86 and CD40 but were unable to support the expansion of either naive or effector/memory CD4(+) T cells. Importantly, in vivo depletion of pDCs revealed that this subset was dispensable for either maintenance or regulation of the hepatic Th2 effector response during acute S. mansoni infection. Our data provides strong evidence that S. mansoni infection favors the establishment of an immunogenic, rather than tolerogenic, liver microenvironment that conditions cDCs to initiate and maintain Th2 immunity in the context of ongoing antigen exposure.

KW - Animals

KW - Antigens, Helminth

KW - Cell Differentiation

KW - Cells, Cultured

KW - Dendritic Cells

KW - Liver

KW - Lymphocyte Activation

KW - Mice

KW - Mice, Inbred C57BL

KW - Schistosoma mansoni

KW - Schistosomiasis mansoni

KW - Th2 Cells

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/icb.2015.114

DO - 10.1038/icb.2015.114

M3 - Journal article

C2 - 26657145

VL - 94

SP - 400

EP - 410

JO - Immunology and Cell Biology

JF - Immunology and Cell Biology

IS - 4

ER -