Literature DB >> 28433429

Immunological function of Langerhans cells in HIV infection.

Takamitsu Matsuzawa1, Youichi Ogawa2, Kohji Moriishi3, Shinji Shimada1, Tatsuyoshi Kawamura1.   

Abstract

BACKGROUND: Langerhans cells (LCs) are one of the initial target cells for HIV following sexual exposure and they are productively infected by HIV. HIV-infected LCs migrate to the draining lymph nodes (dLNs) and transmit the virus to CD4+ T cells, leading to the dissemination of HIV. In contrast with the role of LCs in initial HIV acquisition, little is known about the modulation of immune responses by HIV-infected LCs.
OBJECTIVE: We aimed to elucidate the induction of HIV-specific CD8+ T cells and regulatory T cells (Tregs), both of which play important roles in regulating the progression of HIV infection.
METHODS: We examined the inducibility of HLA-A*0201 restricted HIV-specific CD8+ T cells and Tregs by HIV-primed LCs or HIV-primed dendritic cells (DCs) as a control.
RESULTS: The number of HIV-specific CD8+ T cells induced by HIV-primed monocyte-derived LCs (mLCs) was significantly higher than that by HIV-primed monocyte-derived DCs (mDCs). Additionally, HIV-specific CD8+ T cells induced by HIV-primed mLCs produced more IFN-γ than HIV-nonspecific CD8+ T cells. HIV-primed human epidermal LCs also induced IFN-γ-producing HIV-specific CD8+ T cells. As for the induction of Tregs, HIV-primed mLCs and human epidermal LCs significantly impaired the induction of FoxP3hiCD45RA- effector Tregs than HIV-unprimed mLCs and human epidermal LCs.
CONCLUSIONS: HIV-primed LCs trigger beneficial immune responses against HIV infection through the increased induction of HIV-specific CD8+ T cells and the decreased induction of effector Tregs in the initial phase of HIV infection, thereby contributing to the prolonged onset of AIDS.
Copyright © 2017 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  CTLs; HIV; Langerhans cells; Tregs

Mesh:

Substances:

Year:  2017        PMID: 28433429     DOI: 10.1016/j.jdermsci.2017.03.015

Source DB:  PubMed          Journal:  J Dermatol Sci        ISSN: 0923-1811            Impact factor:   4.563


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