Epithelial adhesion molecules can inhibit HIV-1–specific CD8+ T-cell functions

Under persistent antigenic stimulation, virus-specific CD8+ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 inf...

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Published inBlood Vol. 117; no. 19; pp. 5112 - 5122
Main Authors Streeck, Hendrik, Kwon, Douglas S., Pyo, Augustine, Flanders, Michael, Chevalier, Mathieu F., Law, Kenneth, Jülg, Boris, Trocha, Kasper, Jolin, Jonathan S., Anahtar, Melis N., Lian, Jeff, Toth, Ildiko, Brumme, Zabrina, Chang, J. Judy, Caron, Tyler, Rodig, Scott J., Milner, Danny A., Piechoka-Trocha, Alicja, Kaufmann, Daniel E., Walker, Bruce D., Altfeld, Marcus
Format Journal Article
LanguageEnglish
Published Washington, DC Elsevier Inc 12.05.2011
Americain Society of Hematology
American Society of Hematology
Subjects
Biological and medical sciences
Cadherins - immunology
Cadherins - metabolism
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - metabolism
Cell Adhesion Molecules - immunology
Cell Adhesion Molecules - metabolism
Cell Separation
Colon - immunology
Colon - metabolism
Enzyme-Linked Immunosorbent Assay
Female
Flow Cytometry
Fluorescent Antibody Technique
Hematologic and hematopoietic diseases
HIV Infections - immunology
HIV Infections - metabolism
HIV-1 - immunology
Human viral diseases
Humans
Immunobiology
Immunohistochemistry
Immunology
Infectious diseases
Lectins, C-Type - biosynthesis
Lectins, C-Type - immunology
Life Sciences
Lymphocyte Activation - immunology
Male
Medical sciences
Receptors, Immunologic
Trans-Activators - biosynthesis
Trans-Activators - immunology
Vascular Biology
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Virus Replication - immunology
Immunopathology
Hematology
HIV-1 virus
Cell adhesion molecule
Retroviridae
AIDS
Immune deficiency
Lentivirus
Infection
Virus
Viral disease
Inhibitor
Human immunodeficiency virus
CD8 T lymphocyte
Online AccessGet full text
ISSN0006-4971
1528-0020
1528-0020
DOI10.1182/blood-2010-12-321588

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Abstract Under persistent antigenic stimulation, virus-specific CD8+ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 infection have significantly elevated KLRG1 expression (P < .001); show abnormal distribution of E-cadherin, the natural ligand of KLRG1, in the intestinal mucosa; and have elevated levels of systemic soluble E-cadherin (sE-cadherin) that significantly correlate with HIV-1 viral load (R = 0.7, P = .004). We furthermore demonstrate that in the presence of sE-cadherin, KLRG1hi HIV-1–specific CD8+ T cells are impaired in their ability to respond by cytokine secretion on antigenic stimulation (P = .002) and to inhibit viral replication (P = .03) in vitro. Thus, these data suggest a critical mechanism by which the disruption of the intestinal epithelium associated with HIV-1 leads to increased systemic levels of sE-cadherin, which inhibits the effector functions of KLRG1hi-expressing HIV-1–specific CD8+ T cells systemically.
AbstractList Under persistent antigenic stimulation, virus-specific CD8⁺ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 infection have significantly elevated KLRG1 expression (P < .001); show abnormal distribution of E-cadherin, the natural ligand of KLRG1, in the intestinal mucosa; and have elevated levels of systemic soluble E-cadherin (sE-cadherin) that significantly correlate with HIV-1 viral load (R = 0.7, P = .004). We furthermore demonstrate that in the presence of sE-cadherin, KLRG1(hi) HIV-1-specific CD8⁺ T cells are impaired in their ability to respond by cytokine secretion on antigenic stimulation (P = .002) and to inhibit viral replication (P = .03) in vitro. Thus, these data suggest a critical mechanism by which the disruption of the intestinal epithelium associated with HIV-1 leads to increased systemic levels of sE-cadherin, which inhibits the effector functions of KLRG1(hi)-expressing HIV-1-specific CD8⁺ T cells systemically.
Under persistent antigenic stimulation, virus-specific CD8+ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 infection have significantly elevated KLRG1 expression (P < .001); show abnormal distribution of E-cadherin, the natural ligand of KLRG1, in the intestinal mucosa; and have elevated levels of systemic soluble E-cadherin (sE-cadherin) that significantly correlate with HIV-1 viral load (R = 0.7, P = .004). We furthermore demonstrate that in the presence of sE-cadherin, KLRG1hi HIV-1–specific CD8+ T cells are impaired in their ability to respond by cytokine secretion on antigenic stimulation (P = .002) and to inhibit viral replication (P = .03) in vitro. Thus, these data suggest a critical mechanism by which the disruption of the intestinal epithelium associated with HIV-1 leads to increased systemic levels of sE-cadherin, which inhibits the effector functions of KLRG1hi-expressing HIV-1–specific CD8+ T cells systemically.
Under persistent antigenic stimulation, virus-specific CD8⁺ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 infection have significantly elevated KLRG1 expression (P < .001); show abnormal distribution of E-cadherin, the natural ligand of KLRG1, in the intestinal mucosa; and have elevated levels of systemic soluble E-cadherin (sE-cadherin) that significantly correlate with HIV-1 viral load (R = 0.7, P = .004). We furthermore demonstrate that in the presence of sE-cadherin, KLRG1(hi) HIV-1-specific CD8⁺ T cells are impaired in their ability to respond by cytokine secretion on antigenic stimulation (P = .002) and to inhibit viral replication (P = .03) in vitro. Thus, these data suggest a critical mechanism by which the disruption of the intestinal epithelium associated with HIV-1 leads to increased systemic levels of sE-cadherin, which inhibits the effector functions of KLRG1(hi)-expressing HIV-1-specific CD8⁺ T cells systemically.Under persistent antigenic stimulation, virus-specific CD8⁺ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 infection have significantly elevated KLRG1 expression (P < .001); show abnormal distribution of E-cadherin, the natural ligand of KLRG1, in the intestinal mucosa; and have elevated levels of systemic soluble E-cadherin (sE-cadherin) that significantly correlate with HIV-1 viral load (R = 0.7, P = .004). We furthermore demonstrate that in the presence of sE-cadherin, KLRG1(hi) HIV-1-specific CD8⁺ T cells are impaired in their ability to respond by cytokine secretion on antigenic stimulation (P = .002) and to inhibit viral replication (P = .03) in vitro. Thus, these data suggest a critical mechanism by which the disruption of the intestinal epithelium associated with HIV-1 leads to increased systemic levels of sE-cadherin, which inhibits the effector functions of KLRG1(hi)-expressing HIV-1-specific CD8⁺ T cells systemically.
Author Jolin, Jonathan S.
Lian, Jeff
Caron, Tyler
Flanders, Michael
Trocha, Kasper
Chevalier, Mathieu F.
Rodig, Scott J.
Jülg, Boris
Milner, Danny A.
Piechoka-Trocha, Alicja
Walker, Bruce D.
Anahtar, Melis N.
Chang, J. Judy
Streeck, Hendrik
Law, Kenneth
Kwon, Douglas S.
Toth, Ildiko
Kaufmann, Daniel E.
Altfeld, Marcus
Pyo, Augustine
Brumme, Zabrina
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Issue 19
Keywords Immunopathology
Hematology
HIV-1 virus
Cell adhesion molecule
Retroviridae
AIDS
Immune deficiency
Lentivirus
Infection
Virus
Viral disease
Inhibitor
Human immunodeficiency virus
CD8 T lymphocyte
Language English
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CC BY 4.0
Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
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Snippet Under persistent antigenic stimulation, virus-specific CD8+ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as...
Under persistent antigenic stimulation, virus-specific CD8⁺ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as...
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SubjectTerms Biological and medical sciences
Cadherins - immunology
Cadherins - metabolism
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - metabolism
Cell Adhesion Molecules - immunology
Cell Adhesion Molecules - metabolism
Cell Separation
Colon - immunology
Colon - metabolism
Enzyme-Linked Immunosorbent Assay
Female
Flow Cytometry
Fluorescent Antibody Technique
Hematologic and hematopoietic diseases
HIV Infections - immunology
HIV Infections - metabolism
HIV-1 - immunology
Human viral diseases
Humans
Immunobiology
Immunohistochemistry
Immunology
Infectious diseases
Lectins, C-Type - biosynthesis
Lectins, C-Type - immunology
Life Sciences
Lymphocyte Activation - immunology
Male
Medical sciences
Receptors, Immunologic
Trans-Activators - biosynthesis
Trans-Activators - immunology
Vascular Biology
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Virus Replication - immunology
Title Epithelial adhesion molecules can inhibit HIV-1–specific CD8+ T-cell functions
URI https://dx.doi.org/10.1182/blood-2010-12-321588
https://www.ncbi.nlm.nih.gov/pubmed/21403126
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https://pubmed.ncbi.nlm.nih.gov/PMC3109536
https://ashpublications.org/blood/article-pdf/117/19/5112/1335505/zh801911005112.pdf
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