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Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression

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Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression. / Calcinotto, Arianna; Brevi, Arianna; Chesi, Marta; Ferrarese, Roberto; Garcia Perez, Laura; Grioni, Matteo; Kumar, Shaji; Garbitt, Victoria M; Sharik, Meaghen E; Henderson, Kimberly J; Tonon, Giovanni; Tomura, Michio; Miwa, Yoshihiro; Esplugues, Enric; Flavell, Richard A; Huber, Samuel; Canducci, Filippo; Rajkumar, Vincent S; Bergsagel, P Leif; Bellone, Matteo.

In: NAT COMMUN, Vol. 9, 03.12.2018, p. 4832.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Calcinotto, A, Brevi, A, Chesi, M, Ferrarese, R, Garcia Perez, L, Grioni, M, Kumar, S, Garbitt, VM, Sharik, ME, Henderson, KJ, Tonon, G, Tomura, M, Miwa, Y, Esplugues, E, Flavell, RA, Huber, S, Canducci, F, Rajkumar, VS, Bergsagel, PL & Bellone, M 2018, 'Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression', NAT COMMUN, vol. 9, pp. 4832. https://doi.org/10.1038/s41467-018-07305-8

APA

Calcinotto, A., Brevi, A., Chesi, M., Ferrarese, R., Garcia Perez, L., Grioni, M., Kumar, S., Garbitt, V. M., Sharik, M. E., Henderson, K. J., Tonon, G., Tomura, M., Miwa, Y., Esplugues, E., Flavell, R. A., Huber, S., Canducci, F., Rajkumar, V. S., Bergsagel, P. L., & Bellone, M. (2018). Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression. NAT COMMUN, 9, 4832. https://doi.org/10.1038/s41467-018-07305-8

Vancouver

Calcinotto A, Brevi A, Chesi M, Ferrarese R, Garcia Perez L, Grioni M et al. Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression. NAT COMMUN. 2018 Dec 3;9:4832. https://doi.org/10.1038/s41467-018-07305-8

Bibtex

@article{5ba4fc9c4d124bcdb8307507260960a2,
title = "Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression",
abstract = "The gut microbiota has been causally linked to cancer, yet how intestinal microbes influence progression of extramucosal tumors is poorly understood. Here we provide evidence implying that Prevotella heparinolytica promotes the differentiation of Th17 cells colonizing the gut and migrating to the bone marrow (BM) of transgenic Vk*MYC mice, where they favor progression of multiple myeloma (MM). Lack of IL-17 in Vk*MYC mice, or disturbance of their microbiome delayed MM appearance. Similarly, in smoldering MM patients, higher levels of BM IL-17 predicted faster disease progression. IL-17 induced STAT3 phosphorylation in murine plasma cells, and activated eosinophils. Treatment of Vk*MYC mice with antibodies blocking IL-17, IL-17RA, and IL-5 reduced BM accumulation of Th17 cells and eosinophils and delayed disease progression. Thus, in Vk*MYC mice, commensal bacteria appear to unleash a paracrine signaling network between adaptive and innate immunity that accelerates progression to MM, and can be targeted by already available therapies.",
keywords = "Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural",
author = "Arianna Calcinotto and Arianna Brevi and Marta Chesi and Roberto Ferrarese and {Garcia Perez}, Laura and Matteo Grioni and Shaji Kumar and Garbitt, {Victoria M} and Sharik, {Meaghen E} and Henderson, {Kimberly J} and Giovanni Tonon and Michio Tomura and Yoshihiro Miwa and Enric Esplugues and Flavell, {Richard A} and Samuel Huber and Filippo Canducci and Rajkumar, {Vincent S} and Bergsagel, {P Leif} and Matteo Bellone",
year = "2018",
month = dec,
day = "3",
doi = "10.1038/s41467-018-07305-8",
language = "English",
volume = "9",
pages = "4832",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression

AU - Calcinotto, Arianna

AU - Brevi, Arianna

AU - Chesi, Marta

AU - Ferrarese, Roberto

AU - Garcia Perez, Laura

AU - Grioni, Matteo

AU - Kumar, Shaji

AU - Garbitt, Victoria M

AU - Sharik, Meaghen E

AU - Henderson, Kimberly J

AU - Tonon, Giovanni

AU - Tomura, Michio

AU - Miwa, Yoshihiro

AU - Esplugues, Enric

AU - Flavell, Richard A

AU - Huber, Samuel

AU - Canducci, Filippo

AU - Rajkumar, Vincent S

AU - Bergsagel, P Leif

AU - Bellone, Matteo

PY - 2018/12/3

Y1 - 2018/12/3

N2 - The gut microbiota has been causally linked to cancer, yet how intestinal microbes influence progression of extramucosal tumors is poorly understood. Here we provide evidence implying that Prevotella heparinolytica promotes the differentiation of Th17 cells colonizing the gut and migrating to the bone marrow (BM) of transgenic Vk*MYC mice, where they favor progression of multiple myeloma (MM). Lack of IL-17 in Vk*MYC mice, or disturbance of their microbiome delayed MM appearance. Similarly, in smoldering MM patients, higher levels of BM IL-17 predicted faster disease progression. IL-17 induced STAT3 phosphorylation in murine plasma cells, and activated eosinophils. Treatment of Vk*MYC mice with antibodies blocking IL-17, IL-17RA, and IL-5 reduced BM accumulation of Th17 cells and eosinophils and delayed disease progression. Thus, in Vk*MYC mice, commensal bacteria appear to unleash a paracrine signaling network between adaptive and innate immunity that accelerates progression to MM, and can be targeted by already available therapies.

AB - The gut microbiota has been causally linked to cancer, yet how intestinal microbes influence progression of extramucosal tumors is poorly understood. Here we provide evidence implying that Prevotella heparinolytica promotes the differentiation of Th17 cells colonizing the gut and migrating to the bone marrow (BM) of transgenic Vk*MYC mice, where they favor progression of multiple myeloma (MM). Lack of IL-17 in Vk*MYC mice, or disturbance of their microbiome delayed MM appearance. Similarly, in smoldering MM patients, higher levels of BM IL-17 predicted faster disease progression. IL-17 induced STAT3 phosphorylation in murine plasma cells, and activated eosinophils. Treatment of Vk*MYC mice with antibodies blocking IL-17, IL-17RA, and IL-5 reduced BM accumulation of Th17 cells and eosinophils and delayed disease progression. Thus, in Vk*MYC mice, commensal bacteria appear to unleash a paracrine signaling network between adaptive and innate immunity that accelerates progression to MM, and can be targeted by already available therapies.

KW - Journal Article

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

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

U2 - 10.1038/s41467-018-07305-8

DO - 10.1038/s41467-018-07305-8

M3 - SCORING: Journal article

C2 - 30510245

VL - 9

SP - 4832

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

ER -