Gut-associated IgA+ immune cells regulate obesity-related insulin resistance

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Standard

Gut-associated IgA+ immune cells regulate obesity-related insulin resistance. / Luck, Helen; Khan, Saad; Kim, Justin H; Copeland, Julia K; Revelo, Xavier S; Tsai, Sue; Chakraborty, Mainak; Cheng, Kathleen; Tao Chan, Yi; Nøhr, Mark K; Clemente-Casares, Xavier; Perry, Marie-Christine; Ghazarian, Magar; Lei, Helena; Lin, Yi-Hsuan; Coburn, Bryan; Okrainec, Allan; Jackson, Timothy; Poutanen, Susan; Gaisano, Herbert; Allard, Johane P; Guttman, David S; Conner, Margaret E; Winer, Shawn; Winer, Daniel A.

I: Nature Communications, Bind 10, Nr. 1, 3650, 2019.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Luck, H, Khan, S, Kim, JH, Copeland, JK, Revelo, XS, Tsai, S, Chakraborty, M, Cheng, K, Tao Chan, Y, Nøhr, MK, Clemente-Casares, X, Perry, M-C, Ghazarian, M, Lei, H, Lin, Y-H, Coburn, B, Okrainec, A, Jackson, T, Poutanen, S, Gaisano, H, Allard, JP, Guttman, DS, Conner, ME, Winer, S & Winer, DA 2019, 'Gut-associated IgA+ immune cells regulate obesity-related insulin resistance', Nature Communications, bind 10, nr. 1, 3650. https://doi.org/10.1038/s41467-019-11370-y

APA

Luck, H., Khan, S., Kim, J. H., Copeland, J. K., Revelo, X. S., Tsai, S., Chakraborty, M., Cheng, K., Tao Chan, Y., Nøhr, M. K., Clemente-Casares, X., Perry, M-C., Ghazarian, M., Lei, H., Lin, Y-H., Coburn, B., Okrainec, A., Jackson, T., Poutanen, S., ... Winer, D. A. (2019). Gut-associated IgA+ immune cells regulate obesity-related insulin resistance. Nature Communications, 10(1), [3650]. https://doi.org/10.1038/s41467-019-11370-y

Vancouver

Luck H, Khan S, Kim JH, Copeland JK, Revelo XS, Tsai S o.a. Gut-associated IgA+ immune cells regulate obesity-related insulin resistance. Nature Communications. 2019;10(1). 3650. https://doi.org/10.1038/s41467-019-11370-y

Author

Luck, Helen ; Khan, Saad ; Kim, Justin H ; Copeland, Julia K ; Revelo, Xavier S ; Tsai, Sue ; Chakraborty, Mainak ; Cheng, Kathleen ; Tao Chan, Yi ; Nøhr, Mark K ; Clemente-Casares, Xavier ; Perry, Marie-Christine ; Ghazarian, Magar ; Lei, Helena ; Lin, Yi-Hsuan ; Coburn, Bryan ; Okrainec, Allan ; Jackson, Timothy ; Poutanen, Susan ; Gaisano, Herbert ; Allard, Johane P ; Guttman, David S ; Conner, Margaret E ; Winer, Shawn ; Winer, Daniel A. / Gut-associated IgA+ immune cells regulate obesity-related insulin resistance. I: Nature Communications. 2019 ; Bind 10, Nr. 1.

Bibtex

@article{3812b08a36724ad39248f1b20b1e4377,
title = "Gut-associated IgA+ immune cells regulate obesity-related insulin resistance",
abstract = "The intestinal immune system is emerging as an important contributor to obesity-related insulin resistance, but the role of intestinal B cells in this context is unclear. Here, we show that high fat diet (HFD) feeding alters intestinal IgA+ immune cells and that IgA is a critical immune regulator of glucose homeostasis. Obese mice have fewer IgA+ immune cells and less secretory IgA and IgA-promoting immune mediators. HFD-fed IgA-deficient mice have dysfunctional glucose metabolism, a phenotype that can be recapitulated by adoptive transfer of intestinal-associated pan-B cells. Mechanistically, IgA is a crucial link that controls intestinal and adipose tissue inflammation, intestinal permeability, microbial encroachment and the composition of the intestinal microbiome during HFD. Current glucose-lowering therapies, including metformin, affect intestinal-related IgA+ B cell populations in mice, while bariatric surgery regimen alters the level of fecal secretory IgA in humans. These findings identify intestinal IgA+ immune cells as mucosal mediators of whole-body glucose regulation in diet-induced metabolic disease.",
author = "Helen Luck and Saad Khan and Kim, {Justin H} and Copeland, {Julia K} and Revelo, {Xavier S} and Sue Tsai and Mainak Chakraborty and Kathleen Cheng and {Tao Chan}, Yi and N{\o}hr, {Mark K} and Xavier Clemente-Casares and Marie-Christine Perry and Magar Ghazarian and Helena Lei and Yi-Hsuan Lin and Bryan Coburn and Allan Okrainec and Timothy Jackson and Susan Poutanen and Herbert Gaisano and Allard, {Johane P} and Guttman, {David S} and Conner, {Margaret E} and Shawn Winer and Winer, {Daniel A}",
year = "2019",
doi = "10.1038/s41467-019-11370-y",
language = "English",
volume = "10",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Gut-associated IgA+ immune cells regulate obesity-related insulin resistance

AU - Luck, Helen

AU - Khan, Saad

AU - Kim, Justin H

AU - Copeland, Julia K

AU - Revelo, Xavier S

AU - Tsai, Sue

AU - Chakraborty, Mainak

AU - Cheng, Kathleen

AU - Tao Chan, Yi

AU - Nøhr, Mark K

AU - Clemente-Casares, Xavier

AU - Perry, Marie-Christine

AU - Ghazarian, Magar

AU - Lei, Helena

AU - Lin, Yi-Hsuan

AU - Coburn, Bryan

AU - Okrainec, Allan

AU - Jackson, Timothy

AU - Poutanen, Susan

AU - Gaisano, Herbert

AU - Allard, Johane P

AU - Guttman, David S

AU - Conner, Margaret E

AU - Winer, Shawn

AU - Winer, Daniel A

PY - 2019

Y1 - 2019

N2 - The intestinal immune system is emerging as an important contributor to obesity-related insulin resistance, but the role of intestinal B cells in this context is unclear. Here, we show that high fat diet (HFD) feeding alters intestinal IgA+ immune cells and that IgA is a critical immune regulator of glucose homeostasis. Obese mice have fewer IgA+ immune cells and less secretory IgA and IgA-promoting immune mediators. HFD-fed IgA-deficient mice have dysfunctional glucose metabolism, a phenotype that can be recapitulated by adoptive transfer of intestinal-associated pan-B cells. Mechanistically, IgA is a crucial link that controls intestinal and adipose tissue inflammation, intestinal permeability, microbial encroachment and the composition of the intestinal microbiome during HFD. Current glucose-lowering therapies, including metformin, affect intestinal-related IgA+ B cell populations in mice, while bariatric surgery regimen alters the level of fecal secretory IgA in humans. These findings identify intestinal IgA+ immune cells as mucosal mediators of whole-body glucose regulation in diet-induced metabolic disease.

AB - The intestinal immune system is emerging as an important contributor to obesity-related insulin resistance, but the role of intestinal B cells in this context is unclear. Here, we show that high fat diet (HFD) feeding alters intestinal IgA+ immune cells and that IgA is a critical immune regulator of glucose homeostasis. Obese mice have fewer IgA+ immune cells and less secretory IgA and IgA-promoting immune mediators. HFD-fed IgA-deficient mice have dysfunctional glucose metabolism, a phenotype that can be recapitulated by adoptive transfer of intestinal-associated pan-B cells. Mechanistically, IgA is a crucial link that controls intestinal and adipose tissue inflammation, intestinal permeability, microbial encroachment and the composition of the intestinal microbiome during HFD. Current glucose-lowering therapies, including metformin, affect intestinal-related IgA+ B cell populations in mice, while bariatric surgery regimen alters the level of fecal secretory IgA in humans. These findings identify intestinal IgA+ immune cells as mucosal mediators of whole-body glucose regulation in diet-induced metabolic disease.

U2 - 10.1038/s41467-019-11370-y

DO - 10.1038/s41467-019-11370-y

M3 - Journal article

C2 - 31409776

VL - 10

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 3650

ER -

ID: 225793011