PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15274362-8 2004 CONCLUSION: The preadministration of CY enhances IL-12 production in tumor tissues and shifts the cytokine profile to the dominant Th1 type. Cyclophosphamide 37-39 negative elongation factor complex member C/D, Th1l Mus musculus 131-134 28527347-2 2017 Plumieride restores the suppressed cell mediated, humoral immune response and also enhances the release of TNF- alpha, IFN-gamma, and IL-2 (Th-1) in immune compromised cyclosporine and cyclophosphamide treated balb/c mice. Cyclophosphamide 185-201 negative elongation factor complex member C/D, Th1l Mus musculus 140-144 28713366-7 2017 However, when the proposed scheme was complemented by pretreatment with a low dose of CY, we noticed high MC38 TGI together with decreased number of MDSCs in tumor and induction of Th1-type response. Cyclophosphamide 86-88 negative elongation factor complex member C/D, Th1l Mus musculus 181-184 21649551-5 2012 Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5). Cyclophosphamide 23-26 negative elongation factor complex member C/D, Th1l Mus musculus 55-58 21649551-6 2012 MMW irradiation of CPA-treated groups up-regulated the production of Th1 cytokines suppressed by CPA. Cyclophosphamide 19-22 negative elongation factor complex member C/D, Th1l Mus musculus 69-72 21649551-6 2012 MMW irradiation of CPA-treated groups up-regulated the production of Th1 cytokines suppressed by CPA. Cyclophosphamide 97-100 negative elongation factor complex member C/D, Th1l Mus musculus 69-72 21649551-7 2012 Treatment of the CPA+MMW group with selective kappa (kappa) ORA further potentiated this effect of MMWs on Th1 cytokine production, whereas treatment with mu or delta ORA increased the imbalance of cytokine production in the Th2 direction. Cyclophosphamide 17-20 negative elongation factor complex member C/D, Th1l Mus musculus 107-110 28975621-1 2018 The antitumor effectiveness of cyclophosphamide (CTX) and other chemotherapeutics was shown to rely not only on direct cytotoxicity but also on immunogenic tumor cell death and systemic immunomodulatory mechanisms, including regulatory T cell (Treg) depletion, Th1 cell polarization, type I interferon (IFN) and proinflammatory cytokine production. Cyclophosphamide 31-47 negative elongation factor complex member C/D, Th1l Mus musculus 261-264 27924862-7 2016 Furthermore, both cyclophosphamide and ASC treatment significantly decreased the ratio of Th1/Th2 compared with the saline-treatment. Cyclophosphamide 18-34 negative elongation factor complex member C/D, Th1l Mus musculus 90-93 27924862-10 2016 Thus, treatment with cyclophosphamide or ASC can change miRNAs and decrease miR-96-5p and miR-182-5p expression, as well as decreasing the CD138 proportion and the Th1/Th2 ratio, which might be involved in the therapeutic mechanism. Cyclophosphamide 21-37 negative elongation factor complex member C/D, Th1l Mus musculus 164-167 9222642-0 1997 Suppression of cyclophosphamide induced diabetes development and pancreatic Th1 reactivity in NOD mice treated with the interleukin (IL)-12 antagonist IL-12(p40)2. Cyclophosphamide 15-31 negative elongation factor complex member C/D, Th1l Mus musculus 76-79 10585754-9 1999 Thus, the acceleration of diabetes by CY seems to be a complex event, which includes the relatively high resistance of IFN-gamma producers to the drug, their rapid reconstitution, and a Th1 shift of surviving T cell clones. Cyclophosphamide 38-40 negative elongation factor complex member C/D, Th1l Mus musculus 186-189 9579368-0 1998 Cyclophosphamide given after active specific immunization augments antitumor immunity by modulation of Th1 commitment of CD4+ T cells. Cyclophosphamide 0-16 negative elongation factor complex member C/D, Th1l Mus musculus 103-106 9579368-7 1998 CONCLUSIONS: These results suggest that the protective immunity induced by ASI was augmented through the modification of the Th1 and Th2 balance by CPA injection after ASI. Cyclophosphamide 148-151 negative elongation factor complex member C/D, Th1l Mus musculus 125-128 9218751-6 1997 We conclude that cyclophosphamide induces a systemic shift in antigen presenting cells towards favouring Th1 responses, in an MHC dependent manner. Cyclophosphamide 17-33 negative elongation factor complex member C/D, Th1l Mus musculus 105-108 14556668-8 2003 We also demonstrated that Th1-cell therapy is greatly augmented by combination therapy with cyclophosphamide treatment. Cyclophosphamide 92-108 negative elongation factor complex member C/D, Th1l Mus musculus 26-29 12021842-4 2002 Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice. Cyclophosphamide 60-76 negative elongation factor complex member C/D, Th1l Mus musculus 103-106 9833936-8 1998 A selective downregulation of Th1-type cytokine expression was observed in a second set of experiments in which diabetes development was synchronised by cyclophosphamide. Cyclophosphamide 153-169 negative elongation factor complex member C/D, Th1l Mus musculus 30-33 8706342-9 1996 After peptide challenge of splenocytes in vitro, protection against CY-accelerated diabetes was associated with higher peptide-specific production of T helper type 2 (Th2)-associated interleukins 4 and 10, whereas Th1-associated interferon-gamma and IL-2 were proportionally less represented. Cyclophosphamide 68-70 negative elongation factor complex member C/D, Th1l Mus musculus 214-217 8933279-9 1996 Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.). Cyclophosphamide 183-199 negative elongation factor complex member C/D, Th1l Mus musculus 23-26