Systemically dispersed innate IL-13–expressing cells in type 2 immunity

By April E. Price, Hong-Erh Liang, B. Sullivan, R. Reinhardt, C. Eisley, D. Erle, R. Locksley. Proceedings of the National Academy of Sciences of the United States of America, 2010

1,116 citations recorded by the source corpus.

Subfields: Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/27e4ce131a1918412eb17cf7fee147be8f87a7b2

How researchers see this paper

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In Immunology

1. D. Artis
2. R. Locksley
3. S. V. Van Dyken
4. H. Spits
5. A. Mantovani
6. J. Girard
7. A. Chawla
8. C. Cayrol

In Surgery

1. D. Artis
2. C. Cayrol
3. J. Girard
4. Andrew N. J. McKenzie
5. H. Spits
6. R. Locksley
7. A. Mantovani
8. Dan R. Littman

Citations in the corpus

• Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages (2013, background): “Thus, the SVF of perigonadal adipose tissue contains innate lymphoid cells with the phenotype of pre viously described ILC2s (Moro et al., 2010; Neill et al., 2010; Price et al., 2010). without IL5 (Mishra et al., 1999; Kopf et al., 1996).”
• Group 2 Innate Lymphoid Cells Are Critical for the Initiation of Adaptive T Helper 2 Cell-Mediated Allergic Lung Inflammation (2014, background): “, 2013), recently discovered in the gut (Moro et al., 2010; Neill et al., 2010; Price et al., 2010) and airway mucosa of mice (Chang et al.”
• A role for IL-25 and IL-33–driven type-2 innate lymphoid cells in atopic dermatitis (2013, background): “…these cells respond to IL-25 and IL-33 by producing type 2 cytokines, and in mice ILC2s have been shown to induce goblet cell hyperplasia and eosinophilia , and contribute to protection against helminth infections (Moro et al., 2010; Neill et al., 2010; Price et al., 2010; Spits and Cupedo, 2012).”
• Progressive loss of RORγt expression confers distinct functional fates to natural killer cell receptor-expressing RORγt+ innate lymphocytes (2010, positive): “In addition to natural killer (NK) cells, two additional innate lymphocyte subsets have been described: lymphoid tissue inducer (LTi) cells and natural helper cells (also known as type 2 innate lymphocytes or nuocytes) (Moro et al., 2010; Neill et al., 2010; Price et al., 2010).”
• Activated Type 2 Innate Lymphoid Cells regulate Beige Fat Biogenesis (2014, positive): “ILC2s, which are present in lymphoid and nonlymphoid tissues (Moro et al., 2010; Neill et al., 2010; Price et al., 2010),”
• Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation. (2012, background): “They are also Lin , but Sca-1 , CD122lo, heterogeneous for c-kit expression, and express high baseline Il4 transcript, unlike LNH cells (Price et al., 2010).”
• The transcription factor GATA3 controls cell fate and maintenance of type 2 innate lymphoid cells (2012, positive): “We tested our hypothesis that GATA-3 is the lineagedefining transcription factor of ILC2s by examining GATA-3 expression by CD25Sca1 or CD127Sca1 cells among CD3 CD19 cells, marker combinations widely used to ‘‘define’’ ILC2s (Moro et al., 2010; Neill et al., 2010; Price et al., 2010; Saenz et al., ”
• MHCII-Mediated Dialog between Group 2 Innate Lymphoid Cells and CD4+ T Cells Potentiates Type 2 Immunity and Promotes Parasitic Helminth Expulsion (2014, background): “Innate lymphoid cells (ILCs) also play key roles in type-2 responses by producing high amounts of type-2 cytokines (Moro et al., 2010; Neill et al., 2010; Price et al., 2010).”
• Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus (2011, background): “These cells are activated in response to the epithelial cell–derived cytokines IL-25 and/or IL-33 and can promote T H 2 cytokine–dependent protective immunity to helminth parasite”
• IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy. (2014, background): “After infection with the helminth Nippostrongylus brasi-liensis and in response to IL-33, ILC2s expanded robustly and produced large amounts of IL-13, which led to goblet cell hyperplasia in the intestine and worm expulsion, even in the absence of adaptive immunity [7 – 9].”