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Inflammation-induced formation of fat-associated lymphoid clusters

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Inflammation-induced formation of fat-associated lymphoid clusters. / Bénézech, Cécile; Luu, Nguyet-Thin; Walker, Jennifer A et al.
In: Nature Immunology, Vol. 16, No. 8, 29.06.2015, p. 819-828.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Bénézech, C, Luu, N-T, Walker, JA, Kruglov, AA, Loo, Y, Nakamura, K, Zhang, Y, Nayar, S, Jones, LH, Flores-Langarica, A, McIntosh, A, Marshall, J, Barone, F, Besra, G, Miles, K, Allen, JE, Gray, M, Kollias, G, Cunningham, AF, Withers, DR, Toellner, KM, Jones, ND, Veldhoen, M, Nedospasov, SA, McKenzie, ANJ & Caamaño, JH 2015, 'Inflammation-induced formation of fat-associated lymphoid clusters', Nature Immunology, vol. 16, no. 8, pp. 819-828. https://doi.org/10.1038/ni.3215

APA

Bénézech, C., Luu, N-T., Walker, J. A., Kruglov, A. A., Loo, Y., Nakamura, K., Zhang, Y., Nayar, S., Jones, L. H., Flores-Langarica, A., McIntosh, A., Marshall, J., Barone, F., Besra, G., Miles, K., Allen, J. E., Gray, M., Kollias, G., Cunningham, A. F., ... Caamaño, J. H. (2015). Inflammation-induced formation of fat-associated lymphoid clusters. Nature Immunology, 16(8), 819-828. https://doi.org/10.1038/ni.3215

Vancouver

Bénézech C, Luu N-T, Walker JA, Kruglov AA, Loo Y, Nakamura K et al. Inflammation-induced formation of fat-associated lymphoid clusters. Nature Immunology. 2015 Jun 29;16(8):819-828. doi: 10.1038/ni.3215

Author

Bénézech, Cécile ; Luu, Nguyet-Thin ; Walker, Jennifer A et al. / Inflammation-induced formation of fat-associated lymphoid clusters. In: Nature Immunology. 2015 ; Vol. 16, No. 8. pp. 819-828.

Bibtex

@article{8f63ef0c770145abb3cc54f002bd333f,
title = "Inflammation-induced formation of fat-associated lymphoid clusters",
abstract = "Fat-associated lymphoid clusters (FALCs) are a type of lymphoid tissue associated with visceral fat. Here we found that the distribution of FALCs was heterogeneous, with the pericardium containing large numbers of these clusters. FALCs contributed to the retention of B-1 cells in the peritoneal cavity through high expression of the chemokine CXCL13, and they supported B cell proliferation and germinal center differentiation during peritoneal immunological challenges. FALC formation was induced by inflammation, which triggered the recruitment of myeloid cells that expressed tumor-necrosis factor (TNF) necessary for signaling via the TNF receptors in stromal cells. Natural killer T cells (NKT cells) restricted by the antigen-presenting molecule CD1d were likewise required for the inducible formation of FALCs. Thus, FALCs supported and coordinated the activation of innate B cells and T cells during serosal immune responses. ",
keywords = "Animals, B-Lymphocytes, Chemokine CXCL13, Flow Cytometry, Gene Expression, Inflammation, Intra-Abdominal Fat, Lymphocytes, Lymphoid Tissue, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Microscopy, Confocal, Myeloid Cells, Natural Killer T-Cells, Receptors, Tumor Necrosis Factor, Reverse Transcriptase Polymerase Chain Reaction, Stromal Cells, Tumor Necrosis Factor-alpha, Journal Article, Research Support, Non-U.S. Gov't",
author = "C{\'e}cile B{\'e}n{\'e}zech and Nguyet-Thin Luu and Walker, {Jennifer A} and Kruglov, {Andrei A} and Yunhua Loo and Kyoko Nakamura and Yang Zhang and Saba Nayar and Jones, {Lucy H} and Adriana Flores-Langarica and Alistair McIntosh and Jennifer Marshall and Francesca Barone and Gurdyal Besra and Katherine Miles and Allen, {Judith E} and Mohini Gray and George Kollias and Cunningham, {Adam F} and Withers, {David R} and Toellner, {Kai Michael} and Jones, {Nick D} and Marc Veldhoen and Nedospasov, {Sergei A} and McKenzie, {Andrew N J} and Caama{\~n}o, {Jorge H}",
year = "2015",
month = jun,
day = "29",
doi = "10.1038/ni.3215",
language = "English",
volume = "16",
pages = "819--828",
journal = "Nature Immunology",
issn = "1529-2908",
publisher = "Nature Publishing Group",
number = "8",

}

RIS

TY - JOUR

T1 - Inflammation-induced formation of fat-associated lymphoid clusters

AU - Bénézech, Cécile

AU - Luu, Nguyet-Thin

AU - Walker, Jennifer A

AU - Kruglov, Andrei A

AU - Loo, Yunhua

AU - Nakamura, Kyoko

AU - Zhang, Yang

AU - Nayar, Saba

AU - Jones, Lucy H

AU - Flores-Langarica, Adriana

AU - McIntosh, Alistair

AU - Marshall, Jennifer

AU - Barone, Francesca

AU - Besra, Gurdyal

AU - Miles, Katherine

AU - Allen, Judith E

AU - Gray, Mohini

AU - Kollias, George

AU - Cunningham, Adam F

AU - Withers, David R

AU - Toellner, Kai Michael

AU - Jones, Nick D

AU - Veldhoen, Marc

AU - Nedospasov, Sergei A

AU - McKenzie, Andrew N J

AU - Caamaño, Jorge H

PY - 2015/6/29

Y1 - 2015/6/29

N2 - Fat-associated lymphoid clusters (FALCs) are a type of lymphoid tissue associated with visceral fat. Here we found that the distribution of FALCs was heterogeneous, with the pericardium containing large numbers of these clusters. FALCs contributed to the retention of B-1 cells in the peritoneal cavity through high expression of the chemokine CXCL13, and they supported B cell proliferation and germinal center differentiation during peritoneal immunological challenges. FALC formation was induced by inflammation, which triggered the recruitment of myeloid cells that expressed tumor-necrosis factor (TNF) necessary for signaling via the TNF receptors in stromal cells. Natural killer T cells (NKT cells) restricted by the antigen-presenting molecule CD1d were likewise required for the inducible formation of FALCs. Thus, FALCs supported and coordinated the activation of innate B cells and T cells during serosal immune responses.

AB - Fat-associated lymphoid clusters (FALCs) are a type of lymphoid tissue associated with visceral fat. Here we found that the distribution of FALCs was heterogeneous, with the pericardium containing large numbers of these clusters. FALCs contributed to the retention of B-1 cells in the peritoneal cavity through high expression of the chemokine CXCL13, and they supported B cell proliferation and germinal center differentiation during peritoneal immunological challenges. FALC formation was induced by inflammation, which triggered the recruitment of myeloid cells that expressed tumor-necrosis factor (TNF) necessary for signaling via the TNF receptors in stromal cells. Natural killer T cells (NKT cells) restricted by the antigen-presenting molecule CD1d were likewise required for the inducible formation of FALCs. Thus, FALCs supported and coordinated the activation of innate B cells and T cells during serosal immune responses.

KW - Animals

KW - B-Lymphocytes

KW - Chemokine CXCL13

KW - Flow Cytometry

KW - Gene Expression

KW - Inflammation

KW - Intra-Abdominal Fat

KW - Lymphocytes

KW - Lymphoid Tissue

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Microscopy, Confocal

KW - Myeloid Cells

KW - Natural Killer T-Cells

KW - Receptors, Tumor Necrosis Factor

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Stromal Cells

KW - Tumor Necrosis Factor-alpha

KW - Journal Article

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

U2 - 10.1038/ni.3215

DO - 10.1038/ni.3215

M3 - Journal article

C2 - 26147686

VL - 16

SP - 819

EP - 828

JO - Nature Immunology

JF - Nature Immunology

SN - 1529-2908

IS - 8

ER -