Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer

Matteo Bellone; Arianna Brevi; Samuel Huber

doi:10.1128/MMBR.00064-19

Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer

Standard

Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer. / Bellone, Matteo; Brevi, Arianna; Huber, Samuel.

in: MICROBIOL MOL BIOL R, Jahrgang 84, Nr. 2, 20.05.2020.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung

Harvard

Bellone, M, Brevi, A & Huber, S 2020, 'Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer', MICROBIOL MOL BIOL R, Jg. 84, Nr. 2. https://doi.org/10.1128/MMBR.00064-19

APA

Bellone, M., Brevi, A., & Huber, S. (2020). Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer. MICROBIOL MOL BIOL R, 84(2). https://doi.org/10.1128/MMBR.00064-19

Vancouver

Bellone M, Brevi A, Huber S. Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer. MICROBIOL MOL BIOL R. 2020 Mai 20;84(2). https://doi.org/10.1128/MMBR.00064-19

Bibtex

@article{01b1d07629a34a8f868824de83472222,

title = "Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer",

abstract = "Technologies allowing genetic sequencing of the human microbiome are opening new realms to discovery. The host microbiota substantially impacts immune responses both in immune-mediated inflammatory diseases (IMIDs) and in tumors affecting tissues beyond skin and mucosae. However, a mechanistic link between host microbiota and cancer or IMIDs has not been well established. Here, we propose T helper 17 (TH17) lymphocytes as the connecting factor between host microbiota and rheumatoid or psoriatic arthritides, multiple sclerosis, breast or ovarian cancer, and multiple myeloma. We theorize that similar mechanisms favor the expansion of gut-borne TH17 cells and their deployment at the site of inflammation in extraborder IMIDs and tumors, where TH17 cells are driving forces. Thus, from a pathogenic standpoint, tumors may share mechanistic routes with IMIDs. A review of similarities and divergences in microbiota-TH17 cell interactions in IMIDs and cancer sheds light on previously ignored pathways in either one of the two groups of pathologies and identifies novel therapeutic avenues.",

author = "Matteo Bellone and Arianna Brevi and Samuel Huber",

note = "Copyright {\textcopyright} 2020 American Society for Microbiology.",

year = "2020",

month = may,

day = "20",

doi = "10.1128/MMBR.00064-19",

language = "English",

volume = "84",

journal = "MICROBIOL MOL BIOL R",

issn = "1092-2172",

publisher = "American Society for Microbiology",

number = "2",

}

RIS

TY - JOUR

T1 - Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer

AU - Bellone, Matteo

AU - Brevi, Arianna

AU - Huber, Samuel

PY - 2020/5/20

Y1 - 2020/5/20

N2 - Technologies allowing genetic sequencing of the human microbiome are opening new realms to discovery. The host microbiota substantially impacts immune responses both in immune-mediated inflammatory diseases (IMIDs) and in tumors affecting tissues beyond skin and mucosae. However, a mechanistic link between host microbiota and cancer or IMIDs has not been well established. Here, we propose T helper 17 (TH17) lymphocytes as the connecting factor between host microbiota and rheumatoid or psoriatic arthritides, multiple sclerosis, breast or ovarian cancer, and multiple myeloma. We theorize that similar mechanisms favor the expansion of gut-borne TH17 cells and their deployment at the site of inflammation in extraborder IMIDs and tumors, where TH17 cells are driving forces. Thus, from a pathogenic standpoint, tumors may share mechanistic routes with IMIDs. A review of similarities and divergences in microbiota-TH17 cell interactions in IMIDs and cancer sheds light on previously ignored pathways in either one of the two groups of pathologies and identifies novel therapeutic avenues.

AB - Technologies allowing genetic sequencing of the human microbiome are opening new realms to discovery. The host microbiota substantially impacts immune responses both in immune-mediated inflammatory diseases (IMIDs) and in tumors affecting tissues beyond skin and mucosae. However, a mechanistic link between host microbiota and cancer or IMIDs has not been well established. Here, we propose T helper 17 (TH17) lymphocytes as the connecting factor between host microbiota and rheumatoid or psoriatic arthritides, multiple sclerosis, breast or ovarian cancer, and multiple myeloma. We theorize that similar mechanisms favor the expansion of gut-borne TH17 cells and their deployment at the site of inflammation in extraborder IMIDs and tumors, where TH17 cells are driving forces. Thus, from a pathogenic standpoint, tumors may share mechanistic routes with IMIDs. A review of similarities and divergences in microbiota-TH17 cell interactions in IMIDs and cancer sheds light on previously ignored pathways in either one of the two groups of pathologies and identifies novel therapeutic avenues.

U2 - 10.1128/MMBR.00064-19

DO - 10.1128/MMBR.00064-19

M3 - SCORING: Review article

C2 - 32132244

VL - 84

JO - MICROBIOL MOL BIOL R

JF - MICROBIOL MOL BIOL R

SN - 1092-2172

IS - 2

ER -