scholarly journals Group 3 innate lymphoid cells mediate intestinal selection of commensal bacteria-specific CD4+ T cells

Science ◽  
2015 ◽  
Vol 348 (6238) ◽  
pp. 1031-1035 ◽  
Author(s):  
M. R. Hepworth ◽  
T. C. Fung ◽  
S. H. Masur ◽  
J. R. Kelsen ◽  
F. M. McConnell ◽  
...  
2014 ◽  
Vol 7 (5) ◽  
pp. 1045-1057 ◽  
Author(s):  
L L Korn ◽  
H L Thomas ◽  
H G Hubbeling ◽  
S P Spencer ◽  
R Sinha ◽  
...  

2020 ◽  
Author(s):  
Wan-Chung Hu

Human host immune responses to parasitic infections are complex. They can be categorized into four immunological pathways against four types of parasitic infections. For intracellular protozoa, the eradicable host immunological pathway is TH1 immunity involving macrophages, interferon gamma (IFNg) CD4 T cells, innate lymphoid cells 1 (ILC1), CD8 T cells, invariant natural killer T cells 1 (iNKT1) cells, and immunoglobulin G3 (IgG3) B cells. For free-living extracellular protozoa, the eradicable host immunological pathway is TH22 immunity involving neutrophils, interleukin (IL)-22/IL-17 CD4 T cells, innate lymphoid cells 3 (ILC3), iNKT17 cells, and IgG2 B cells. For endoparasites (helminths), the eradicable host immunological pathway is TH2a immunity with inflammatory eosinophils (iEOS), IL-5/IL-4 CD4 T cells, IL-25 inducing inflammatory innate lymphoid cells 2 (iILC2), mast cells-tryptase (MCt), iNKT2 cells, and IgG4 B cells. For ectoparasites (parasitic insects and arachnids), the eradicable host immunological pathway is TH2b immunity with inflammatory basophils, mast cells-tryptase/chymase (MCtc), IL-3/IL-4 CD4 T cells, IL-33 inducing nature innate lymphoid cells 2 (nILC2), iNKT2 cells, and immunoglobulin E (IgE) B cells. The tolerable host immunity against ectoparasites and endoparasites is TH9 immunity with regulatory eosinophils, regulatory basophils, IL-9 mast cells (MMC9), thymic stromal lymphopoietin inducing innate lymphoid cells 2, IL-9 CD4 T cells, iNKT2 cells, and IgA2 B cells. This categorization provides a complete framework of immunological pathways against four types of parasitic infections.


2018 ◽  
Vol 56 (01) ◽  
pp. E2-E89
Author(s):  
K Neumann ◽  
M Schoedsack ◽  
S Steinmann ◽  
A Ochel ◽  
P Breda ◽  
...  

2012 ◽  
Vol 209 (9) ◽  
pp. 1595-1609 ◽  
Author(s):  
Margherita Coccia ◽  
Oliver J. Harrison ◽  
Chris Schiering ◽  
Mark J. Asquith ◽  
Burkhard Becher ◽  
...  

Although very high levels of interleukin (IL)-1β are present in the intestines of patients suffering from inflammatory bowel diseases (IBD), little is known about the contribution of IL-1β to intestinal pathology. Here, we used two complementary models of chronic intestinal inflammation to address the role of IL-1β in driving innate and adaptive pathology in the intestine. We show that IL-1β promotes innate immune pathology in Helicobacter hepaticus–triggered intestinal inflammation by augmenting the recruitment of granulocytes and the accumulation and activation of innate lymphoid cells (ILCs). Using a T cell transfer colitis model, we demonstrate a key role for T cell–specific IL-1 receptor (IL-1R) signals in the accumulation and survival of pathogenic CD4+ T cells in the colon. Furthermore, we show that IL-1β promotes Th17 responses from CD4+ T cells and ILCs in the intestine, and we describe synergistic interactions between IL-1β and IL-23 signals that sustain innate and adaptive inflammatory responses in the gut. These data identify multiple mechanisms through which IL-1β promotes intestinal pathology and suggest that targeting IL-1β may represent a useful therapeutic approach in IBD.


Immunity ◽  
2014 ◽  
Vol 41 (2) ◽  
pp. 283-295 ◽  
Author(s):  
Christopher J. Oliphant ◽  
You Yi Hwang ◽  
Jennifer A. Walker ◽  
Maryam Salimi ◽  
See Heng Wong ◽  
...  

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