tetano
Editor, Senior Moderator
Hum Vaccin Immunother. 2015 Jun 19:0. [Epub ahead of print]
[h=1]Low expression of activation marker CD69 and chemokine receptors CCR5 and CXCR3 on memory T cells after 2009 H1N1 influenza A antigen stimulation in vitro following H1N1 vaccination of HIV-infected individuals.[/h] Chawansuntati K[SUP]1[/SUP], Chotirosniramit N, Sugandhavesa P, Aurpibul L, Thetket S, Kosashunhanan N, Supindham T, Kaewthip O, Sroysuwan P, Sirisanthana T, Suparatpinyo K, Wipasa J.
[h=3]Author information[/h]
[h=3]Abstract[/h] Unlike well-studied antibody responses to pandemic 2009 H1N1 influenza A virus vaccines in human immunodeficiency virus-infected (HIV+) individuals, less well understood are cell-mediated immune (CMI) responses to this antigen in this susceptible population. We investigated such influenza-specific CMI responses in 61 HIV+ individuals and in 20 HIV-negative (HIV-) healthy controls. Each was vaccinated with a single licensed dose of inactivated, split-virion vaccine comprised of the influenza A/California/7/2009 (H1N1) virus-like strain. Cells collected just prior to vaccination and at 1 and 3 months afterwards were stimulated in vitro with dialyzed vaccine antigen and assayed by flow cytometry for cytokines TNF-α, IFN-γ, IL-2, and IL-10, for degranulation marker CD107a, as well as phenotypes of memory T-cell subpopulations. Comparable increases of cytokine-producing and CD107a-expressing T cells were observed in both HIV+ subjects and healthy HIV- controls. However, by 3 months post-vaccination, in vitro antigen stimulation of peripheral blood mononuclear cells induced greater expansion in controls of both CD4 and CD8 central memory and effector memory T cells, as well as higher expression of the activation marker CD69 and chemokine receptors CCR5 and CXCR3 than in HIV+ subjects. We concluded CD4+ and CD8+ memory T cells produce cytokines at comparable levels in both groups, whereas the expression after in vitro stimulation of molecules critical for cell migration to infection sites are lower in the HIV+ than in comparable controls. Further immunization strategies against influenza are needed to improve the CMI responses in people living with HIV.
[h=4]KEYWORDS:[/h] 2009 H1N1 influenza A vaccine; ART, antiretroviral therapy; CCR5, C-C chemokine receptor 5; CMI, cell-mediated immune; CTLA4, cytotoxic T-lymphocyte-associated protein 4; CXCR3, C-X-C chemokine receptor 3; DMSO, Dimethyl sulfoxide; FBS, fetal bovine serum; HAI, hemagglutination inhibitory; HIV, human immunodeficiency virus; HIV-infection; IQR, interquartile range; PBMCs, peripheral blood mononuclear cells; PD1, Programmed cell death protein 1; PHA, phytohaemagglutinin; TCM, central memory T cells; TEM, effector memory T cells; WHO, world health organization; activation markers; cellular immunity; chemokine receptors; immunological memory responses
PMID: 26091502 [PubMed - as supplied by publisher]
[h=1]Low expression of activation marker CD69 and chemokine receptors CCR5 and CXCR3 on memory T cells after 2009 H1N1 influenza A antigen stimulation in vitro following H1N1 vaccination of HIV-infected individuals.[/h] Chawansuntati K[SUP]1[/SUP], Chotirosniramit N, Sugandhavesa P, Aurpibul L, Thetket S, Kosashunhanan N, Supindham T, Kaewthip O, Sroysuwan P, Sirisanthana T, Suparatpinyo K, Wipasa J.
[h=3]Author information[/h]
[h=3]Abstract[/h] Unlike well-studied antibody responses to pandemic 2009 H1N1 influenza A virus vaccines in human immunodeficiency virus-infected (HIV+) individuals, less well understood are cell-mediated immune (CMI) responses to this antigen in this susceptible population. We investigated such influenza-specific CMI responses in 61 HIV+ individuals and in 20 HIV-negative (HIV-) healthy controls. Each was vaccinated with a single licensed dose of inactivated, split-virion vaccine comprised of the influenza A/California/7/2009 (H1N1) virus-like strain. Cells collected just prior to vaccination and at 1 and 3 months afterwards were stimulated in vitro with dialyzed vaccine antigen and assayed by flow cytometry for cytokines TNF-α, IFN-γ, IL-2, and IL-10, for degranulation marker CD107a, as well as phenotypes of memory T-cell subpopulations. Comparable increases of cytokine-producing and CD107a-expressing T cells were observed in both HIV+ subjects and healthy HIV- controls. However, by 3 months post-vaccination, in vitro antigen stimulation of peripheral blood mononuclear cells induced greater expansion in controls of both CD4 and CD8 central memory and effector memory T cells, as well as higher expression of the activation marker CD69 and chemokine receptors CCR5 and CXCR3 than in HIV+ subjects. We concluded CD4+ and CD8+ memory T cells produce cytokines at comparable levels in both groups, whereas the expression after in vitro stimulation of molecules critical for cell migration to infection sites are lower in the HIV+ than in comparable controls. Further immunization strategies against influenza are needed to improve the CMI responses in people living with HIV.
[h=4]KEYWORDS:[/h] 2009 H1N1 influenza A vaccine; ART, antiretroviral therapy; CCR5, C-C chemokine receptor 5; CMI, cell-mediated immune; CTLA4, cytotoxic T-lymphocyte-associated protein 4; CXCR3, C-X-C chemokine receptor 3; DMSO, Dimethyl sulfoxide; FBS, fetal bovine serum; HAI, hemagglutination inhibitory; HIV, human immunodeficiency virus; HIV-infection; IQR, interquartile range; PBMCs, peripheral blood mononuclear cells; PD1, Programmed cell death protein 1; PHA, phytohaemagglutinin; TCM, central memory T cells; TEM, effector memory T cells; WHO, world health organization; activation markers; cellular immunity; chemokine receptors; immunological memory responses
PMID: 26091502 [PubMed - as supplied by publisher]