PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9099937-4 1996 Nasal tolerance to EAMG was accompanied by decreased numbers of AChR-reactive IFN-gamma and IL-4 mRNA-expressing cells, and strong up-regulation of TGF-beta mRNA-positive cells in lymphoid organs compared with non-tolerized EAMG control rats. eamg 19-23 interleukin 4 Rattus norvegicus 92-96 9182902-6 1997 Since IFN-gamma, IL-4 and IL-10 promote the development of EAMG, the low expression of these cytokines might contribute to EAMG resistance in young Lewis rats. eamg 59-63 interleukin 4 Rattus norvegicus 17-21 9099937-6 1996 The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG, and that TGF-beta plays an important role in tolerance induction to EAMG. eamg 97-101 interleukin 4 Rattus norvegicus 39-43 8610980-5 1996 The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG and that TGF-beta plays an important role in tolerance induction to EAMG. eamg 97-101 interleukin 4 Rattus norvegicus 39-43 7520837-6 1994 The results suggest that IFN-gamma, IL-4, and TGF-beta are involved in the development of EAMG, and that TGF-beta is important in the induction of oral tolerance to EAMG. eamg 90-94 interleukin 4 Rattus norvegicus 36-40 7520837-3 1994 Upon in vivo recognition of AChR, popliteal, inguinal, and mesenteric lymph nodes, spleen and thymus of rats with EAMG contained higher levels of IFN-gamma, IL-4, and TGF-beta mRNA-expressing cells compared to CFA-injected control rats, implicating the involvement in EAMG of AChR-reactive Th1 and Th2 cells in parallel. eamg 114-118 interleukin 4 Rattus norvegicus 157-161 7520837-5 1994 Oral tolerance to EAMG was characterized by suppression of the levels of MNC expressing IFN-gamma and IL-4, but augmentation of cells expressing TGF-beta. eamg 18-22 interleukin 4 Rattus norvegicus 102-106