TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection

Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identif...
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Autor*in:	Kong, Ling [verfasserIn] Jiang, Dan [verfasserIn] He, Cheng [verfasserIn] Xia, Jing [verfasserIn] Wei, Haixia [verfasserIn] Zhou, Lijuan [verfasserIn] Peng, Hongjuan [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	ROP18 IL20RB STAT3 Proinflammatory immunity

Übergeordnetes Werk:	Enthalten in: Parasites & vectors - London : BioMed Central, 2008, 13(2020), 1 vom: 07. Aug.
Übergeordnetes Werk:	volume:13 ; year:2020 ; number:1 ; day:07 ; month:08

Links:	Volltext

DOI / URN:	10.1186/s13071-020-04251-7

Katalog-ID:	SPR040592545

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520			\|a Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense.
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700	1		\|a Zhou, Lijuan \|e verfasserin \|4 aut
700	1		\|a Peng, Hongjuan \|e verfasserin \|4 aut
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Indexfelder

author_variant	l k lk d j dj c h ch j x jx h w hw l z lz h p hp
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allfields	10.1186/s13071-020-04251-7 doi (DE-627)SPR040592545 (SPR)s13071-020-04251-7-e DE-627 ger DE-627 rakwb eng 570 ASE Kong, Ling verfasserin aut TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense. ROP18 (dpeaa)DE-He213 IL20RB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Proinflammatory immunity (dpeaa)DE-He213 Jiang, Dan verfasserin aut He, Cheng verfasserin aut Xia, Jing verfasserin aut Wei, Haixia verfasserin aut Zhou, Lijuan verfasserin aut Peng, Hongjuan verfasserin aut Enthalten in Parasites & vectors London : BioMed Central, 2008 13(2020), 1 vom: 07. Aug. (DE-627)558690076 (DE-600)2409480-8 1756-3305 nnns volume:13 year:2020 number:1 day:07 month:08 https://dx.doi.org/10.1186/s13071-020-04251-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2020 1 07 08
spelling	10.1186/s13071-020-04251-7 doi (DE-627)SPR040592545 (SPR)s13071-020-04251-7-e DE-627 ger DE-627 rakwb eng 570 ASE Kong, Ling verfasserin aut TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense. ROP18 (dpeaa)DE-He213 IL20RB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Proinflammatory immunity (dpeaa)DE-He213 Jiang, Dan verfasserin aut He, Cheng verfasserin aut Xia, Jing verfasserin aut Wei, Haixia verfasserin aut Zhou, Lijuan verfasserin aut Peng, Hongjuan verfasserin aut Enthalten in Parasites & vectors London : BioMed Central, 2008 13(2020), 1 vom: 07. Aug. (DE-627)558690076 (DE-600)2409480-8 1756-3305 nnns volume:13 year:2020 number:1 day:07 month:08 https://dx.doi.org/10.1186/s13071-020-04251-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2020 1 07 08
allfields_unstemmed	10.1186/s13071-020-04251-7 doi (DE-627)SPR040592545 (SPR)s13071-020-04251-7-e DE-627 ger DE-627 rakwb eng 570 ASE Kong, Ling verfasserin aut TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense. ROP18 (dpeaa)DE-He213 IL20RB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Proinflammatory immunity (dpeaa)DE-He213 Jiang, Dan verfasserin aut He, Cheng verfasserin aut Xia, Jing verfasserin aut Wei, Haixia verfasserin aut Zhou, Lijuan verfasserin aut Peng, Hongjuan verfasserin aut Enthalten in Parasites & vectors London : BioMed Central, 2008 13(2020), 1 vom: 07. Aug. (DE-627)558690076 (DE-600)2409480-8 1756-3305 nnns volume:13 year:2020 number:1 day:07 month:08 https://dx.doi.org/10.1186/s13071-020-04251-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2020 1 07 08
allfieldsGer	10.1186/s13071-020-04251-7 doi (DE-627)SPR040592545 (SPR)s13071-020-04251-7-e DE-627 ger DE-627 rakwb eng 570 ASE Kong, Ling verfasserin aut TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense. ROP18 (dpeaa)DE-He213 IL20RB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Proinflammatory immunity (dpeaa)DE-He213 Jiang, Dan verfasserin aut He, Cheng verfasserin aut Xia, Jing verfasserin aut Wei, Haixia verfasserin aut Zhou, Lijuan verfasserin aut Peng, Hongjuan verfasserin aut Enthalten in Parasites & vectors London : BioMed Central, 2008 13(2020), 1 vom: 07. Aug. (DE-627)558690076 (DE-600)2409480-8 1756-3305 nnns volume:13 year:2020 number:1 day:07 month:08 https://dx.doi.org/10.1186/s13071-020-04251-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2020 1 07 08
allfieldsSound	10.1186/s13071-020-04251-7 doi (DE-627)SPR040592545 (SPR)s13071-020-04251-7-e DE-627 ger DE-627 rakwb eng 570 ASE Kong, Ling verfasserin aut TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense. ROP18 (dpeaa)DE-He213 IL20RB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Proinflammatory immunity (dpeaa)DE-He213 Jiang, Dan verfasserin aut He, Cheng verfasserin aut Xia, Jing verfasserin aut Wei, Haixia verfasserin aut Zhou, Lijuan verfasserin aut Peng, Hongjuan verfasserin aut Enthalten in Parasites & vectors London : BioMed Central, 2008 13(2020), 1 vom: 07. Aug. (DE-627)558690076 (DE-600)2409480-8 1756-3305 nnns volume:13 year:2020 number:1 day:07 month:08 https://dx.doi.org/10.1186/s13071-020-04251-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2020 1 07 08
language	English
source	Enthalten in Parasites & vectors 13(2020), 1 vom: 07. Aug. volume:13 year:2020 number:1 day:07 month:08
sourceStr	Enthalten in Parasites & vectors 13(2020), 1 vom: 07. Aug. volume:13 year:2020 number:1 day:07 month:08
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	ROP18 IL20RB STAT3 Proinflammatory immunity
dewey-raw	570
isfreeaccess_bool	true
container_title	Parasites & vectors
authorswithroles_txt_mv	Kong, Ling @@aut@@ Jiang, Dan @@aut@@ He, Cheng @@aut@@ Xia, Jing @@aut@@ Wei, Haixia @@aut@@ Zhou, Lijuan @@aut@@ Peng, Hongjuan @@aut@@
publishDateDaySort_date	2020-08-07T00:00:00Z
hierarchy_top_id	558690076
dewey-sort	3570
id	SPR040592545
language_de	englisch
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Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. 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author	Kong, Ling
spellingShingle	Kong, Ling ddc 570 misc ROP18 misc IL20RB misc STAT3 misc Proinflammatory immunity TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection
authorStr	Kong, Ling
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dewey-ones	570 - Life sciences; biology
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topic_title	570 ASE TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection ROP18 (dpeaa)DE-He213 IL20RB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Proinflammatory immunity (dpeaa)DE-He213
topic	ddc 570 misc ROP18 misc IL20RB misc STAT3 misc Proinflammatory immunity
topic_unstemmed	ddc 570 misc ROP18 misc IL20RB misc STAT3 misc Proinflammatory immunity
topic_browse	ddc 570 misc ROP18 misc IL20RB misc STAT3 misc Proinflammatory immunity
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
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hierarchy_parent_title	Parasites & vectors
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title	TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection
ctrlnum	(DE-627)SPR040592545 (SPR)s13071-020-04251-7-e
title_full	TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection
author_sort	Kong, Ling
journal	Parasites & vectors
journalStr	Parasites & vectors
lang_code	eng
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author_browse	Kong, Ling Jiang, Dan He, Cheng Xia, Jing Wei, Haixia Zhou, Lijuan Peng, Hongjuan
container_volume	13
class	570 ASE
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author-letter	Kong, Ling
doi_str_mv	10.1186/s13071-020-04251-7
dewey-full	570
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title_sort	tgrop18 targets il20rb for host-defense-related-stat3 activation during toxoplasma gondii infection
title_auth	TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection
abstract	Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense.
abstractGer	Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense.
abstract_unstemmed	Background Toxoplasma gondii is an opportunistic protozoan infecting almost one-third of the world’s population. Toxoplasma gondii rhoptry protein 18 (TgROP18) is a key virulence factor determining the parasite’s acute virulence and is secreted into host cells during infection. We previously identified the interaction of TgROP18 and host cell immune-related receptor protein IL20RB, and observed the activation of STAT3 in human keratinocytes (HaCaT) cells infected by the rop16 knockout RH strain, though TgROP16 is regarded as being responsible for host STAT3 activation during T. gondii invasion. Therefore, we hypothesize TgROP18 can activate host STAT3 through binding to IL20RB. Methods CRISPR-CAS9 technology was used to generate the ROP16 and ROP18 double knockout RH strain, RH-∆rop16∆rop18. SDS-PAGE and western blot were used to detect STAT3 activation in different HaCaT cells with high endogenous IL20RB expression treated with T. gondii tachyzoites infection, recombinant ROP18, or IL-20. FRET and co-immunoprecipitation (Co-IP) was used to detect the protein-protein interaction. Results We observed that TgROP18 was involved in a synergic activation of the host JAK/STAT3 pathway together with TgROP16 in human HaCaT cells infected with T. gondii or treated with recombinant TgROP18 protein, stimulating host proinflammatory immune responses such as expression of TNF-α. The effect of recombinant ROP18 on STAT3 phosphorylation was presented in a dose-dependent manner. Additionally, TgROP18 was identified to target IL20RB on its extracellular domain. When we treated different cell lines with the recombinant ROP18, STAT3 phosphorylation could only be observed in the cells with endogenous IL20RB expression, such as HaCaT cells. Conclusions These findings indicate that TgROP18-IL20RB interaction upon T. gondii invasion was involved in STAT3 activation, which is associated with host cell defense.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	1
title_short	TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection
url	https://dx.doi.org/10.1186/s13071-020-04251-7
remote_bool	true
author2	Jiang, Dan He, Cheng Xia, Jing Wei, Haixia Zhou, Lijuan Peng, Hongjuan
author2Str	Jiang, Dan He, Cheng Xia, Jing Wei, Haixia Zhou, Lijuan Peng, Hongjuan
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doi_str	10.1186/s13071-020-04251-7
up_date	2024-07-03T16:59:31.322Z
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