Langerhans cells in HIV-1 infection

G. Stingl, K. Rappersberger, E. Tschachler, S. Gartner, V. Groh, D. L. Mann, K. Wolff, M. Popovic

Research output: Contribution to journalArticle

Abstract

The skin-specific immune surveillance system protects against invading microorganisms and transformed cells expressing tumor-specific neoantigens. This system includes antigen-presenting Langerhans cells, dermal and epidermal T lymphocytes, cytokine-producing keratinocytes, and draining peripheral lymph nodes. In patients infected with human immunodeficiency virus-1 (HIV-1), this surveillance system appears to be compromised, as evidenced by a reduction in the epidermal Langerhans cell population. Because human epidermal Langerhans cell express surface-bound CD4 antigens, HLA-DR antigens, and Fc-IgG receptors, all of which are involved in HIV-1 binding to, or entry into, the target cell, the reduction in Langerhans cells in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) may be a direct consequence of HIV-1 infection and subsequent injury to Langerhans cells. Detailed ultrastructural studies have confirmed moderate to severe morphologic damage in some Langerhans cells of such patients and the presence of HIV-1-like particles on Langerhans cell surface membranes and in the extracellular spaces. The biologic consequences of Langerhans cell infection by HIV-1 could be either impaired antigen presentation function of viable Langerhans cells or possible transmission of the retrovirus to the T-cell compartment in skin or lymph nodes, with subsequent depletion of CD4+ T cells via widespread syncytia formation between HIV-1-infected and noninfected cells. The facts that herpes simplex virus, specific cytokines, and ultraviolet B radiation can activate signals for HIV-1 expression and that epidermal cells can elaborate large amounts of cytokines, particularly with enhanced ultraviolet B exposure, may have important clinical implications for HIV-1-infected patients.

Original languageEnglish (US)
Pages (from-to)1210-1217
Number of pages8
JournalJournal of the American Academy of Dermatology
Volume22
Issue number6 II SUPPL.
StatePublished - 1990
Externally publishedYes

Fingerprint

Langerhans Cells
Virus Diseases
HIV-1
Cytokines
T-Lymphocytes
Skin
Acquired Immunodeficiency Syndrome
Lymph Nodes
IgG Receptors
Virus Attachment
CD4 Antigens
Fc Receptors
Antigen Presentation
Extracellular Space
HLA-DR Antigens
Antigen-Presenting Cells
Simplexvirus
Giant Cells
Retroviridae
Keratinocytes

ASJC Scopus subject areas

  • Dermatology

Cite this

Stingl, G., Rappersberger, K., Tschachler, E., Gartner, S., Groh, V., Mann, D. L., ... Popovic, M. (1990). Langerhans cells in HIV-1 infection. Journal of the American Academy of Dermatology, 22(6 II SUPPL.), 1210-1217.

Langerhans cells in HIV-1 infection. / Stingl, G.; Rappersberger, K.; Tschachler, E.; Gartner, S.; Groh, V.; Mann, D. L.; Wolff, K.; Popovic, M.

In: Journal of the American Academy of Dermatology, Vol. 22, No. 6 II SUPPL., 1990, p. 1210-1217.

Research output: Contribution to journalArticle

Stingl, G, Rappersberger, K, Tschachler, E, Gartner, S, Groh, V, Mann, DL, Wolff, K & Popovic, M 1990, 'Langerhans cells in HIV-1 infection', Journal of the American Academy of Dermatology, vol. 22, no. 6 II SUPPL., pp. 1210-1217.
Stingl G, Rappersberger K, Tschachler E, Gartner S, Groh V, Mann DL et al. Langerhans cells in HIV-1 infection. Journal of the American Academy of Dermatology. 1990;22(6 II SUPPL.):1210-1217.
Stingl, G. ; Rappersberger, K. ; Tschachler, E. ; Gartner, S. ; Groh, V. ; Mann, D. L. ; Wolff, K. ; Popovic, M. / Langerhans cells in HIV-1 infection. In: Journal of the American Academy of Dermatology. 1990 ; Vol. 22, No. 6 II SUPPL. pp. 1210-1217.
@article{ab02d82aeca34335ae4a1360bc6b5b1b,
title = "Langerhans cells in HIV-1 infection",
abstract = "The skin-specific immune surveillance system protects against invading microorganisms and transformed cells expressing tumor-specific neoantigens. This system includes antigen-presenting Langerhans cells, dermal and epidermal T lymphocytes, cytokine-producing keratinocytes, and draining peripheral lymph nodes. In patients infected with human immunodeficiency virus-1 (HIV-1), this surveillance system appears to be compromised, as evidenced by a reduction in the epidermal Langerhans cell population. Because human epidermal Langerhans cell express surface-bound CD4 antigens, HLA-DR antigens, and Fc-IgG receptors, all of which are involved in HIV-1 binding to, or entry into, the target cell, the reduction in Langerhans cells in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) may be a direct consequence of HIV-1 infection and subsequent injury to Langerhans cells. Detailed ultrastructural studies have confirmed moderate to severe morphologic damage in some Langerhans cells of such patients and the presence of HIV-1-like particles on Langerhans cell surface membranes and in the extracellular spaces. The biologic consequences of Langerhans cell infection by HIV-1 could be either impaired antigen presentation function of viable Langerhans cells or possible transmission of the retrovirus to the T-cell compartment in skin or lymph nodes, with subsequent depletion of CD4+ T cells via widespread syncytia formation between HIV-1-infected and noninfected cells. The facts that herpes simplex virus, specific cytokines, and ultraviolet B radiation can activate signals for HIV-1 expression and that epidermal cells can elaborate large amounts of cytokines, particularly with enhanced ultraviolet B exposure, may have important clinical implications for HIV-1-infected patients.",
author = "G. Stingl and K. Rappersberger and E. Tschachler and S. Gartner and V. Groh and Mann, {D. L.} and K. Wolff and M. Popovic",
year = "1990",
language = "English (US)",
volume = "22",
pages = "1210--1217",
journal = "Journal of the American Academy of Dermatology",
issn = "0190-9622",
publisher = "Mosby Inc.",
number = "6 II SUPPL.",

}

TY - JOUR

T1 - Langerhans cells in HIV-1 infection

AU - Stingl, G.

AU - Rappersberger, K.

AU - Tschachler, E.

AU - Gartner, S.

AU - Groh, V.

AU - Mann, D. L.

AU - Wolff, K.

AU - Popovic, M.

PY - 1990

Y1 - 1990

N2 - The skin-specific immune surveillance system protects against invading microorganisms and transformed cells expressing tumor-specific neoantigens. This system includes antigen-presenting Langerhans cells, dermal and epidermal T lymphocytes, cytokine-producing keratinocytes, and draining peripheral lymph nodes. In patients infected with human immunodeficiency virus-1 (HIV-1), this surveillance system appears to be compromised, as evidenced by a reduction in the epidermal Langerhans cell population. Because human epidermal Langerhans cell express surface-bound CD4 antigens, HLA-DR antigens, and Fc-IgG receptors, all of which are involved in HIV-1 binding to, or entry into, the target cell, the reduction in Langerhans cells in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) may be a direct consequence of HIV-1 infection and subsequent injury to Langerhans cells. Detailed ultrastructural studies have confirmed moderate to severe morphologic damage in some Langerhans cells of such patients and the presence of HIV-1-like particles on Langerhans cell surface membranes and in the extracellular spaces. The biologic consequences of Langerhans cell infection by HIV-1 could be either impaired antigen presentation function of viable Langerhans cells or possible transmission of the retrovirus to the T-cell compartment in skin or lymph nodes, with subsequent depletion of CD4+ T cells via widespread syncytia formation between HIV-1-infected and noninfected cells. The facts that herpes simplex virus, specific cytokines, and ultraviolet B radiation can activate signals for HIV-1 expression and that epidermal cells can elaborate large amounts of cytokines, particularly with enhanced ultraviolet B exposure, may have important clinical implications for HIV-1-infected patients.

AB - The skin-specific immune surveillance system protects against invading microorganisms and transformed cells expressing tumor-specific neoantigens. This system includes antigen-presenting Langerhans cells, dermal and epidermal T lymphocytes, cytokine-producing keratinocytes, and draining peripheral lymph nodes. In patients infected with human immunodeficiency virus-1 (HIV-1), this surveillance system appears to be compromised, as evidenced by a reduction in the epidermal Langerhans cell population. Because human epidermal Langerhans cell express surface-bound CD4 antigens, HLA-DR antigens, and Fc-IgG receptors, all of which are involved in HIV-1 binding to, or entry into, the target cell, the reduction in Langerhans cells in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) may be a direct consequence of HIV-1 infection and subsequent injury to Langerhans cells. Detailed ultrastructural studies have confirmed moderate to severe morphologic damage in some Langerhans cells of such patients and the presence of HIV-1-like particles on Langerhans cell surface membranes and in the extracellular spaces. The biologic consequences of Langerhans cell infection by HIV-1 could be either impaired antigen presentation function of viable Langerhans cells or possible transmission of the retrovirus to the T-cell compartment in skin or lymph nodes, with subsequent depletion of CD4+ T cells via widespread syncytia formation between HIV-1-infected and noninfected cells. The facts that herpes simplex virus, specific cytokines, and ultraviolet B radiation can activate signals for HIV-1 expression and that epidermal cells can elaborate large amounts of cytokines, particularly with enhanced ultraviolet B exposure, may have important clinical implications for HIV-1-infected patients.

UR - http://www.scopus.com/inward/record.url?scp=0025311521&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025311521&partnerID=8YFLogxK

M3 - Article

C2 - 2193948

AN - SCOPUS:0025311521

VL - 22

SP - 1210

EP - 1217

JO - Journal of the American Academy of Dermatology

JF - Journal of the American Academy of Dermatology

SN - 0190-9622

IS - 6 II SUPPL.

ER -