Cross-talk between type 3 innate lymphoid cells and the gut microbiota in inflammatory bowel disease

被引:38
作者
Buela, Kristine-Ann G. [1 ]
Omenetti, Sara [1 ]
Pizarro, Theresa T. [1 ]
机构
[1] Case Western Reserve Univ, Sch Med, Dept Pathol, Cleveland, OH 44106 USA
基金
美国国家卫生研究院;
关键词
gut microbiota; inflammatory bowel disease; innate lymphoid cells; mucosal immunity; NATURAL-KILLER-CELLS; ARYL-HYDROCARBON RECEPTOR; ROR-GAMMA-T; INTESTINAL INFLAMMATION; DENDRITIC CELLS; COMMENSAL MICROFLORA; TISSUE HOMEOSTASIS; IL-22; IMMUNITY; COLITIS;
D O I
10.1097/MOG.0000000000000217
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Purpose of review Innate lymphoid cells (ILCs) are a newly-identified population of immune cells prevalent in, but not limited to, mucosal tissues that not only play a significant role in immune homeostasis and host defense, but also in disease pathogenesis. This review highlights the importance of type 3 ILCs (ILC3s) and their interactions with the intestinal microflora, both in maintaining gut health and in the development of inflammatory bowel disease (IBD). Recent findings Distinct lineages of ILCs are defined based on the presence of cell surface proteins, secretion of effector cytokines and expression of master transcription factors that determine their differentiation and inflammatory behavior. These ILC subgroups mirror corresponding CD4(+) T-cell subsets, with which they share many phenotypic, morphologic and functional attributes. ILC3s, in particular, through direct and indirect interactions with the gut microbiota, have been identified to promote protection and maintenance of epithelial integrity, as well as to regulate intestinal inflammation and fibrosis, such as that observed in IBD. Summary Gut mucosal ILCs respond to environmental cues, such as diet and microflora composition, which can shape downstream immune function. As such, ILCs represent attractive targets for the development of therapeutic modalities to maintain gut health and to potentially treat IBD.
引用
收藏
页码:449 / 455
页数:7
相关论文
共 75 条
  • [31] Differentiation of Type 1 ILCs from a Common Progenitor to All Helper-like Innate Lymphoid Cell Lineages
    Klose, Christoph S. N.
    Flach, Melanie
    Moehle, Luisa
    Rogell, Leif
    Hoyler, Thomas
    Ebert, Karolina
    Fabiunke, Carola
    Pfeifer, Dietmar
    Sexl, Veronika
    Fonseca-Pereira, Diogo
    Domingues, Rita G.
    Veiga-Fernandes, Henrique
    Arnold, Sebastian J.
    Busslinger, Meinrad
    Dunay, Ildiko R.
    Tanriver, Yakup
    Diefenbach, Andreas
    [J]. CELL, 2014, 157 (02) : 340 - 356
  • [32] Lee JS, 2012, FRONT IMMUNOL, V3, DOI [10.3389/fimmu.2012.00010, 10.3389/fpls.2012.00055]
  • [33] AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch
    Lee, Jacob S.
    Cella, Marina
    McDonald, Keely G.
    Garlanda, Cecilia
    Kennedy, Gregory D.
    Nukaya, Manabu
    Mantovani, Alberto
    Kopan, Raphael
    Bradfield, Christopher A.
    Newberry, Rodney D.
    Colonna, Marco
    [J]. NATURE IMMUNOLOGY, 2012, 13 (02) : 144 - U58
  • [34] Microbiota-induced tertiary lymphoid tissues aggravate inflammatory disease in the absence of RORγt and LTi cells
    Lochner, Matthias
    Ohnmacht, Caspar
    Presley, Laura
    Bruhns, Pierre
    Si-Tahar, Mustapha
    Sawa, Shinichiro
    Eberl, Gerard
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 2011, 208 (01) : 125 - 134
  • [35] CX3CR1+ mononuclear phagocytes support colitis-associated innate lymphoid cell production of IL-22
    Longman, Randy S.
    Diehl, Gretchen E.
    Victorio, Daniel A.
    Huh, Jun R.
    Galan, Carolina
    Miraldi, Emily R.
    Swaminath, Arun
    Bonneau, Richard
    Scherl, Ellen J.
    Littman, Dan R.
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 2014, 211 (08) : 1571 - 1583
  • [36] CCR7-dependent trafficking of RORγ+ ILCs creates a unique microenvironment within mucosal draining lymph nodes
    Mackley, Emma C.
    Houston, Stephanie
    Marriott, Clare L.
    Halford, Emily E.
    Lucas, Beth
    Cerovic, Vuk
    Filbey, Kara J.
    Maizels, Rick M.
    Hepworth, Matthew R.
    Sonnenberg, Gregory F.
    Milling, Simon
    Withers, David R.
    [J]. NATURE COMMUNICATIONS, 2015, 6
  • [37] CX3CR1+ macrophages support IL-22 production by innate lymphoid cells during infection with Citrobacter rodentium
    Manta, C.
    Heupel, E.
    Radulovic, K.
    Rossini, V.
    Garbi, N.
    Riedel, C. U.
    Niess, J. H.
    [J]. MUCOSAL IMMUNOLOGY, 2013, 6 (01) : 177 - 188
  • [38] CX3CR1 regulates intestinal macrophage homeostasis, bacterial translocation, and colitogenic Th17 responses in mice
    Medina-Contreras, Oscar
    Geem, Duke
    Laur, Oskar
    Williams, Ifor R.
    Lira, Sergio A.
    Nusrat, Asma
    Parkos, Charles A.
    Denning, Timothy L.
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2011, 121 (12) : 4787 - 4795
  • [39] Monticelli LA, 2011, NAT IMMUNOL, V12, P1045, DOI [10.1031/ni.2131, 10.1038/ni.2131]
  • [40] Innate production of TH2 cytokines by adipose tissue-associated c-Kit+Sca-1+ lymphoid cells
    Moro, Kazuyo
    Yamada, Taketo
    Tanabe, Masanobu
    Takeuchi, Tsutomu
    Ikawa, Tomokatsu
    Kawamoto, Hiroshi
    Furusawa, Jun-ichi
    Ohtani, Masashi
    Fujii, Hideki
    Koyasu, Shigeo
    [J]. NATURE, 2010, 463 (7280) : 540 - U160