Env-Specific IgA from Viremic HIV-Infected Subjects Compromises Antibody-Dependent Cellular Cytotoxicity

Elucidating the factors that modulate HIV-specific antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunity. The aim of this study was to determine whether IgA could modify the magnitude of ADCC in HIV infection, abrogating its protective role. Plasma sampl...

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Vydané v:	Journal of virology Ročník 90; číslo 2; s. 670
Hlavní autori:	Ruiz, María Julia, Ghiglione, Yanina, Falivene, Juliana, Laufer, Natalia, Holgado, María Pía, Socías, María Eugenia, Cahn, Pedro, Sued, Omar, Giavedoni, Luis, Salomón, Horacio, Gherardi, María Magdalena, Rodríguez, Ana María, Turk, Gabriela
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 15.01.2016
Predmet:	Adult Aged Antibody-Dependent Cell Cytotoxicity Fluorometry HIV Antibodies - immunology HIV Envelope Protein gp120 - immunology HIV Infections - immunology Humans Immunoglobulin A - immunology Male Middle Aged Viremia - immunology Young Adult
ISSN:	1098-5514, 1098-5514
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Abstract	Elucidating the factors that modulate HIV-specific antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunity. The aim of this study was to determine whether IgA could modify the magnitude of ADCC in HIV infection, abrogating its protective role. Plasma samples from 20 HIV-positive (HIV(+)) subjects enrolled during primary HIV infection (PHI), 10 chronically infected subjects (chronic), and 7 elite controllers (EC) were used. ADCC was determined by using a fluorometric ADCC assay, before and after removal of plasma IgA. Data were analyzed by using nonparametric statistics. ADCC was documented in 80% of PHI enrollment samples and in 100% of PHI 12-month, chronic, and EC samples; it peaked after acute infection, reached a plateau in chronic infection, and decreased after initiation of antiretroviral treatment (ART). Significant associations between ADCC and disease progression were found only after removal of plasma IgA from 12-month PHI samples: the magnitude of ADCC not only increased after IgA removal but also correlated with CD4(+) T-cell preservation. This work provides evidence that gp120-specific IgA was capable of modifying ADCC responses during natural HIV infection for the first time and adds to similar evidence provided in other settings. Furthermore, it underscores the complexity of the ADCC phenomenon and will help in an understanding of its underlying mechanisms. Although the induction of ADCC-mediating antibodies in HIV-infected subjects has been extensively documented, the association of these antibodies with protection from disease progression is poorly understood. Here, we demonstrate that plasma IgA is a factor capable of modifying the magnitude of IgG-mediated ADCC in HIV infection, mitigating its beneficial effect. These results help in understanding why previous studies failed to demonstrate correlations between ADCC and disease progression, and they also contribute to the notion that an HIV vaccine should stimulate the production of ADCC-mediating IgG antibodies but not IgA.
AbstractList	Elucidating the factors that modulate HIV-specific antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunity. The aim of this study was to determine whether IgA could modify the magnitude of ADCC in HIV infection, abrogating its protective role. Plasma samples from 20 HIV-positive (HIV(+)) subjects enrolled during primary HIV infection (PHI), 10 chronically infected subjects (chronic), and 7 elite controllers (EC) were used. ADCC was determined by using a fluorometric ADCC assay, before and after removal of plasma IgA. Data were analyzed by using nonparametric statistics. ADCC was documented in 80% of PHI enrollment samples and in 100% of PHI 12-month, chronic, and EC samples; it peaked after acute infection, reached a plateau in chronic infection, and decreased after initiation of antiretroviral treatment (ART). Significant associations between ADCC and disease progression were found only after removal of plasma IgA from 12-month PHI samples: the magnitude of ADCC not only increased after IgA removal but also correlated with CD4(+) T-cell preservation. This work provides evidence that gp120-specific IgA was capable of modifying ADCC responses during natural HIV infection for the first time and adds to similar evidence provided in other settings. Furthermore, it underscores the complexity of the ADCC phenomenon and will help in an understanding of its underlying mechanisms.UNLABELLEDElucidating the factors that modulate HIV-specific antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunity. The aim of this study was to determine whether IgA could modify the magnitude of ADCC in HIV infection, abrogating its protective role. Plasma samples from 20 HIV-positive (HIV(+)) subjects enrolled during primary HIV infection (PHI), 10 chronically infected subjects (chronic), and 7 elite controllers (EC) were used. ADCC was determined by using a fluorometric ADCC assay, before and after removal of plasma IgA. Data were analyzed by using nonparametric statistics. ADCC was documented in 80% of PHI enrollment samples and in 100% of PHI 12-month, chronic, and EC samples; it peaked after acute infection, reached a plateau in chronic infection, and decreased after initiation of antiretroviral treatment (ART). Significant associations between ADCC and disease progression were found only after removal of plasma IgA from 12-month PHI samples: the magnitude of ADCC not only increased after IgA removal but also correlated with CD4(+) T-cell preservation. This work provides evidence that gp120-specific IgA was capable of modifying ADCC responses during natural HIV infection for the first time and adds to similar evidence provided in other settings. Furthermore, it underscores the complexity of the ADCC phenomenon and will help in an understanding of its underlying mechanisms.Although the induction of ADCC-mediating antibodies in HIV-infected subjects has been extensively documented, the association of these antibodies with protection from disease progression is poorly understood. Here, we demonstrate that plasma IgA is a factor capable of modifying the magnitude of IgG-mediated ADCC in HIV infection, mitigating its beneficial effect. These results help in understanding why previous studies failed to demonstrate correlations between ADCC and disease progression, and they also contribute to the notion that an HIV vaccine should stimulate the production of ADCC-mediating IgG antibodies but not IgA.IMPORTANCEAlthough the induction of ADCC-mediating antibodies in HIV-infected subjects has been extensively documented, the association of these antibodies with protection from disease progression is poorly understood. Here, we demonstrate that plasma IgA is a factor capable of modifying the magnitude of IgG-mediated ADCC in HIV infection, mitigating its beneficial effect. These results help in understanding why previous studies failed to demonstrate correlations between ADCC and disease progression, and they also contribute to the notion that an HIV vaccine should stimulate the production of ADCC-mediating IgG antibodies but not IgA. Elucidating the factors that modulate HIV-specific antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunity. The aim of this study was to determine whether IgA could modify the magnitude of ADCC in HIV infection, abrogating its protective role. Plasma samples from 20 HIV-positive (HIV(+)) subjects enrolled during primary HIV infection (PHI), 10 chronically infected subjects (chronic), and 7 elite controllers (EC) were used. ADCC was determined by using a fluorometric ADCC assay, before and after removal of plasma IgA. Data were analyzed by using nonparametric statistics. ADCC was documented in 80% of PHI enrollment samples and in 100% of PHI 12-month, chronic, and EC samples; it peaked after acute infection, reached a plateau in chronic infection, and decreased after initiation of antiretroviral treatment (ART). Significant associations between ADCC and disease progression were found only after removal of plasma IgA from 12-month PHI samples: the magnitude of ADCC not only increased after IgA removal but also correlated with CD4(+) T-cell preservation. This work provides evidence that gp120-specific IgA was capable of modifying ADCC responses during natural HIV infection for the first time and adds to similar evidence provided in other settings. Furthermore, it underscores the complexity of the ADCC phenomenon and will help in an understanding of its underlying mechanisms. Although the induction of ADCC-mediating antibodies in HIV-infected subjects has been extensively documented, the association of these antibodies with protection from disease progression is poorly understood. Here, we demonstrate that plasma IgA is a factor capable of modifying the magnitude of IgG-mediated ADCC in HIV infection, mitigating its beneficial effect. These results help in understanding why previous studies failed to demonstrate correlations between ADCC and disease progression, and they also contribute to the notion that an HIV vaccine should stimulate the production of ADCC-mediating IgG antibodies but not IgA.
Author	Falivene, Juliana Turk, Gabriela Holgado, María Pía Socías, María Eugenia Giavedoni, Luis Ghiglione, Yanina Ruiz, María Julia Rodríguez, Ana María Gherardi, María Magdalena Cahn, Pedro Salomón, Horacio Laufer, Natalia Sued, Omar
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References	21958370 - Viral Immunol. 2011 Oct;24(5):359-68 25125129 - J Virol Methods. 2014 Nov;208:107-14 18353957 - J Virol. 2008 Jun;82(11):5450-9 25499540 - Retrovirology. 2014;11:109 25093660 - PLoS One. 2014;9(8):e104235 11865395 - J Infect Dis. 2002 Feb 15;185(4):439-47 15752839 - Vaccine. 2005 Mar 31;23(19):2522-9 21449728 - Viral Immunol. 2011 Apr;24(2):171-5 15529262 - J Infect Dis. 2004 Dec 1;190(11):1970-8 25856755 - Cell Host Microbe. 2015 Apr 8;17(4):500-6 12960819 - AIDS. 2003 Sep 5;17(13):1871-9 16343526 - J Immunol Methods. 2006 Jan 20;308(1-2):53-67 12884294 - Eur J Immunol. 2003 Aug;33(8):2197-205 22496218 - J Virol. 2012 Jun;86(12):6986-93 3208446 - Clin Exp Immunol. 1988 Sep;73(3):343-7 19124764 - J Immunol. 2009 Jan 15;182(2):1202-10 21543485 - J Virol. 2011 Jul;85(14):7029-36 19414990 - AIDS. 2009 May 15;23(8):897-906 25043633 - Eur J Immunol. 2014 Oct;44(10):2925-37 20874516 - J Infect Dis. 2010 Nov 1;202(9):1444-53 22475592 - N Engl J Med. 2012 Apr 5;366(14):1275-86 22719248 - PLoS Pathog. 2012;8(6):e1002739 24352444 - J Virol. 2014 Mar;88(5):2633-44 24907868 - Lancet. 2014 Jul 19;384(9939):258-71 25941367 - Proc Natl Acad Sci U S A. 2015 May 19;112(20):E2687-94 21831310 - J Int AIDS Soc. 2011;14:40 21792067 - J Acquir Immune Defic Syndr. 2011 Oct 1;58(2):127-31 15896800 - J Immunol Methods. 2005 Jun;301(1-2):89-101 23616666 - J Virol. 2013 Jul;87(13):7445-62 8757343 - J Immunol. 1996 Sep 1;157(5):2168-73 25339767 - J Virol. 2015 Jan;89(1):545-51 24937308 - AIDS. 2014 Aug 24;28(13):1859-70 19843557 - N Engl J Med. 2009 Dec 3;361(23):2209-20 23173935 - Immunology. 2013 Feb;138(2):116-23 3871222 - J Immunol. 1985 Feb;134(2):971-6 23661056 - Proc Natl Acad Sci U S A. 2013 May 28;110(22):9019-24 11435575 - J Virol. 2001 Aug;75(15):6953-61 22674985 - J Virol. 2012 Aug;86(16):8672-80
References_xml	– reference: 19414990 - AIDS. 2009 May 15;23(8):897-906 – reference: 11865395 - J Infect Dis. 2002 Feb 15;185(4):439-47 – reference: 18353957 - J Virol. 2008 Jun;82(11):5450-9 – reference: 22475592 - N Engl J Med. 2012 Apr 5;366(14):1275-86 – reference: 23173935 - Immunology. 2013 Feb;138(2):116-23 – reference: 25043633 - Eur J Immunol. 2014 Oct;44(10):2925-37 – reference: 12884294 - Eur J Immunol. 2003 Aug;33(8):2197-205 – reference: 25499540 - Retrovirology. 2014;11:109 – reference: 3208446 - Clin Exp Immunol. 1988 Sep;73(3):343-7 – reference: 22496218 - J Virol. 2012 Jun;86(12):6986-93 – reference: 20874516 - J Infect Dis. 2010 Nov 1;202(9):1444-53 – reference: 21831310 - J Int AIDS Soc. 2011;14:40 – reference: 25339767 - J Virol. 2015 Jan;89(1):545-51 – reference: 21449728 - Viral Immunol. 2011 Apr;24(2):171-5 – reference: 22674985 - J Virol. 2012 Aug;86(16):8672-80 – reference: 15896800 - J Immunol Methods. 2005 Jun;301(1-2):89-101 – reference: 21958370 - Viral Immunol. 2011 Oct;24(5):359-68 – reference: 23616666 - J Virol. 2013 Jul;87(13):7445-62 – reference: 24937308 - AIDS. 2014 Aug 24;28(13):1859-70 – reference: 25941367 - Proc Natl Acad Sci U S A. 2015 May 19;112(20):E2687-94 – reference: 15752839 - Vaccine. 2005 Mar 31;23(19):2522-9 – reference: 24352444 - J Virol. 2014 Mar;88(5):2633-44 – reference: 8757343 - J Immunol. 1996 Sep 1;157(5):2168-73 – reference: 19124764 - J Immunol. 2009 Jan 15;182(2):1202-10 – reference: 22719248 - PLoS Pathog. 2012;8(6):e1002739 – reference: 19843557 - N Engl J Med. 2009 Dec 3;361(23):2209-20 – reference: 15529262 - J Infect Dis. 2004 Dec 1;190(11):1970-8 – reference: 21543485 - J Virol. 2011 Jul;85(14):7029-36 – reference: 25125129 - J Virol Methods. 2014 Nov;208:107-14 – reference: 12960819 - AIDS. 2003 Sep 5;17(13):1871-9 – reference: 21792067 - J Acquir Immune Defic Syndr. 2011 Oct 1;58(2):127-31 – reference: 23661056 - Proc Natl Acad Sci U S A. 2013 May 28;110(22):9019-24 – reference: 11435575 - J Virol. 2001 Aug;75(15):6953-61 – reference: 3871222 - J Immunol. 1985 Feb;134(2):971-6 – reference: 16343526 - J Immunol Methods. 2006 Jan 20;308(1-2):53-67 – reference: 24907868 - Lancet. 2014 Jul 19;384(9939):258-71 – reference: 25093660 - PLoS One. 2014;9(8):e104235 – reference: 25856755 - Cell Host Microbe. 2015 Apr 8;17(4):500-6
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Snippet	Elucidating the factors that modulate HIV-specific antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunity. The aim...
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SubjectTerms	Adult Aged Antibody-Dependent Cell Cytotoxicity Fluorometry HIV Antibodies - immunology HIV Envelope Protein gp120 - immunology HIV Infections - immunology Humans Immunoglobulin A - immunology Male Middle Aged Viremia - immunology Young Adult
Title	Env-Specific IgA from Viremic HIV-Infected Subjects Compromises Antibody-Dependent Cellular Cytotoxicity
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