a6haiaze

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?:abstract	Severe acute respiratory syndrome coronavirus 2 infections can cause coronavirus disease 2019 (COVID-19), which manifests with a range of severities from mild illness to life-threatening pneumonia and multi-organ failure Severe COVID-19 is characterized by an inflammatory signature, including high levels of inflammatory cytokines, alveolar inflammatory infiltrates and vascular microthrombi Here we show that patients with severe COVID-19 produced a unique serologic signature, including an increased likelihood of IgG1 with afucosylated Fc glycans This Fc modification on severe acute respiratory syndrome coronavirus 2 IgGs enhanced interactions with the activating Fcgamma receptor FcgammaRIIIa;when incorporated into immune complexes, Fc afucosylation enhanced production of inflammatory cytokines by monocytes, including interleukin-6 and tumor necrosis factor These results show that disease severity in COVID-19 correlates with the presence of proinflammatory IgG Fc structures, including afucosylated IgG1 Severe acute respiratory syndrome coronavirus 2 infections can cause coronavirus disease 2019 (COVID-19), which manifests with a range of severities from mild illness to life-threatening pneumonia and multi-organ failure. Severe COVID-19 is characterized by an inflammatory signature, including high levels of inflammatory cytokines, alveolar inflammatory infiltrates and vascular microthrombi. Here we show that patients with severe COVID-19 produced a unique serologic signature, including an increased likelihood of IgG1 with afucosylated Fc glycans. This Fc modification on severe acute respiratory syndrome coronavirus 2 IgGs enhanced interactions with the activating FcÎ³ receptor FcÎ³RIIIa; when incorporated into immune complexes, Fc afucosylation enhanced production of inflammatory cytokines by monocytes, including interleukin-6 and tumor necrosis factor. These results show that disease severity in COVID-19 correlates with the presence of proinflammatory IgG Fc structures, including afucosylated IgG1.
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?:creator	<https://research.tib.eu/covid-19/entity/Chakraborty%2C_S.%3B_Gonzalez%2C_J.%3B_Edwards%2C_K.%3B_Mallajosyula%2C_V.%3B_Buzzanco%2C_A._S.%3B_Sherwood%2C_R.%3B_Buffone%2C_C.%3B_Kathale%2C_N.%3B_Providenza%2C_S.%3B_Xie%2C_M._M.%3B_Andrews%2C_J._R.%3B_Blish%2C_C._A.%3B_Singh%2C_U.%3B_Dugan%2C_H.%3B_Wilson%2C_P._C.%3B_Pham%2C_T._D.%3B_Boyd%2C_S._D.%3B_Nadeau%2C_K._C.%3B_Pinsky%2C_B._A.%3B_Zhang%2C_S.%3B_Memoli%2C_M._J.%3B_Taubenberger%2C_J._K.%3B_Morales%2C_T.%3B_Schapiro%2C_J._M.%3B_Tan%2C_G._S.%3B_Jagannathan%2C_P.%3B_Wang%2C_T._T.> <https://research.tib.eu/covid-19/entity/Chakraborty%2C_Saborni%3B_Gonzalez%2C_Joseph%3B_Edwards%2C_Karlie%3B_Mallajosyula%2C_Vamsee%3B_Buzzanco%2C_Anthony_S%3B_Sherwood%2C_Robert%3B_Buffone%2C_Cindy%3B_Kathale%2C_Nimish%3B_Providenza%2C_Susan%3B_Xie%2C_Markus_M%3B_Andrews%2C_Jason_R%3B_Blish%2C_Catherine_A%3B_Singh%2C_Upinder%3B_Dugan%2C_Haley%3B_Wilson%2C_Patrick_C%3B_Pham%2C_Tho_D%3B_Boyd%2C_Scott_D%3B_Nadeau%2C_Kari_C%3B_Pinsky%2C_Benjamin_A%3B_Zhang%2C_Sheng%3B_Memoli%2C_Matthew_J%3B_Taubenberger%2C_Jeffery_K%3B_Morales%2C_Tasha%3B_Schapiro%2C_Jeffrey_M%3B_Tan%2C_Gene_S%3B_Jagannathan%2C_Prasanna%3B_Wang%2C_Taia_T>
?:journal	Nat_Immunol Nature_Immunology
?:license	unk
?:publication_isRelatedTo_Disease	<https://research.tib.eu/covid-19/entity/COVID-19>
?:source	WHO
?:title	Proinflammatory IgG Fc structures in patients with severe COVID-19
?:type	<https://research.tib.eu/covid-19/vocab/Publication>
?:who_covidence_id	#1065904 #917542
?:year	2021

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?:abstract

Severe acute respiratory syndrome coronavirus 2 infections can cause coronavirus disease 2019 (COVID-19), which manifests with a range of severities from mild illness to life-threatening pneumonia and multi-organ failure Severe COVID-19 is characterized by an inflammatory signature, including high levels of inflammatory cytokines, alveolar inflammatory infiltrates and vascular microthrombi Here we show that patients with severe COVID-19 produced a unique serologic signature, including an increased likelihood of IgG1 with afucosylated Fc glycans This Fc modification on severe acute respiratory syndrome coronavirus 2 IgGs enhanced interactions with the activating Fcgamma receptor FcgammaRIIIa;when incorporated into immune complexes, Fc afucosylation enhanced production of inflammatory cytokines by monocytes, including interleukin-6 and tumor necrosis factor These results show that disease severity in COVID-19 correlates with the presence of proinflammatory IgG Fc structures, including afucosylated IgG1
Severe acute respiratory syndrome coronavirus 2 infections can cause coronavirus disease 2019 (COVID-19), which manifests with a range of severities from mild illness to life-threatening pneumonia and multi-organ failure. Severe COVID-19 is characterized by an inflammatory signature, including high levels of inflammatory cytokines, alveolar inflammatory infiltrates and vascular microthrombi. Here we show that patients with severe COVID-19 produced a unique serologic signature, including an increased likelihood of IgG1 with afucosylated Fc glycans. This Fc modification on severe acute respiratory syndrome coronavirus 2 IgGs enhanced interactions with the activating FcÎ³ receptor FcÎ³RIIIa; when incorporated into immune complexes, Fc afucosylation enhanced production of inflammatory cytokines by monocytes, including interleukin-6 and tumor necrosis factor. These results show that disease severity in COVID-19 correlates with the presence of proinflammatory IgG Fc structures, including afucosylated IgG1.

is ?:annotates of