PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15608148-8	2005	Together, these data indicate that the increased expression of IL-10 significantly contributed to silica-induced lung fibrosis by exacerbating the Th2 response and the production of the profibrotic cytokines IL-4 and IL-13.	Silicon Dioxide	98-104	interleukin 13	Mus musculus	217-222	
18056481-9	2008	In the in vitro assay, a significant increase in TC activation, as defined by surface markers and cytokines, was observed in the cultures containing the silica-exposed macrophages in wild-type and IL-4Ralpha(-/-) mice, with one exception: IL-4Ralpha(-/-) BMdM were unable to induce an increase in IL-13.	Silicon Dioxide	153-159	interleukin 13	Mus musculus	297-302	
16902192-8	2007	However, TNF-alpha, IL-13, monocyte chemotactic protein-1, protease activity, and production of ROS were dose-dependently increased after silica exposure, and production was enhanced after Fc epsilon RI stimulation.	Silicon Dioxide	138-144	interleukin 13	Mus musculus	20-25	
32977946-4	2020	IL-33, but not IL-25 or TSLP, and type 2 cytokines such as IL-5 and IL-13 were critically involved in silica"s exacerbation of OVA-induced airway eosinophilia in mice.	Silicon Dioxide	102-108	interleukin 13	Mus musculus	68-73	
32977946-7	2020	These observations suggest that IL-33 induced in epithelial cells by silica activates ILCs to produce IL-5 and/or IL-13, contributing to silica"s exacerbation of OVA-induced airway eosinophilia in mice.	Silicon Dioxide	69-75	interleukin 13	Mus musculus	114-119	
32977946-7	2020	These observations suggest that IL-33 induced in epithelial cells by silica activates ILCs to produce IL-5 and/or IL-13, contributing to silica"s exacerbation of OVA-induced airway eosinophilia in mice.	Silicon Dioxide	137-143	interleukin 13	Mus musculus	114-119	
32625168-14	2020	Additionally, flunisolide effectively suppressed the responses of proliferation and MCP-1/CCL-2 production from IL-13 stimulated lung fibroblasts from silica- or saline-challenged mice.	Silicon Dioxide	151-157	interleukin 13	Mus musculus	112-117	
24133168-0	2013	IL-13 immunotoxin accelerates resolution of lung pathological changes triggered by silica particles in mice.	Silicon Dioxide	83-89	interleukin 13	Mus musculus	0-5	
24133168-5	2013	Upregulation of IL-13, its receptor subunits IL-13Ralpha1 and IL-13Ralpha2, and shared receptor IL-4Ralpha were associated with development of granulomatous lung inflammation triggered by silica.	Silicon Dioxide	188-194	interleukin 13	Mus musculus	16-21	
24133168-6	2013	IL-13-PE inhibited silica-induced granuloma and fibrotic responses noted at 24 h and 15 d after the last treatment.	Silicon Dioxide	19-25	interleukin 13	Mus musculus	0-5	
24133168-8	2013	In addition, IL-13-PE inhibited both IL-13-induced proliferation of cultured lung fibroblasts from silicotic mice and silica-induced IL-8 generation from A549 cells.	Silicon Dioxide	118-124	interleukin 13	Mus musculus	13-18	
24133168-9	2013	In conclusion, our findings show that therapeutic treatment with IL-13-PE can reverse important pathological features caused by inhalation of silica particles, suggesting that this recombinant immunotoxin is a promising molecular template in drug discovery for the treatment of silicosis.	Silicon Dioxide	142-148	interleukin 13	Mus musculus	65-70