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The Role of Non-classical Regulatory...

Li, Chun.

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The Role of Non-classical Regulatory T Cells in HIV-1 Infection.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The Role of Non-classical Regulatory T Cells in HIV-1 Infection./
作者:	Li, Chun.
面頁冊數:	152 p.
附註:	Source: Dissertation Abstracts International, Volume: 74-06(E), Section: B.
Contained By:	Dissertation Abstracts International74-06B(E).
標題:	Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3553442
ISBN:	9781267929181

The Role of Non-classical Regulatory T Cells in HIV-1 Infection.
Li, Chun.

The Role of Non-classical Regulatory T Cells in HIV-1 Infection. - 152 p.

Source: Dissertation Abstracts International, Volume: 74-06(E), Section: B.

Thesis (Ph.D.)--Harvard University, 2013.

This item is not available from ProQuest Dissertations & Theses.

Regulatory T cells represent a specialized subpopulation of T lymphocytes that may modulate spontaneous HIV-1 disease progression by suppressing immune activation or inhibiting antiviral T cell immune responses. While effects of classical CD25hiFoxP3+CD4+ regulatory T cells during HIV-1 infection have been analyzed in a series of recent investigations, very little is known about the role of non-classical regulatory T cells that do not express intracellular FoxP3. Here I evaluated two groups of non-classical Treg cells. One is phenotypically identified by the surface expression of HLA-G, an HLA class Ib molecule. The other Treg cell population is characterized by the surface expression of latency-associated peptide (LAP), a membrane-bound form of TGF-beta. Both HLA-G and LAP-expressing T cells are present in small proportions in peripheral blood of healthy individuals.

ISBN: 9781267929181Subjects--Topical Terms:

611031
Immunology.

The Role of Non-classical Regulatory T Cells in HIV-1 Infection.
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500 $a Advisers: Bruce D. Walker; Xu G. Yu.
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520 $a Regulatory T cells represent a specialized subpopulation of T lymphocytes that may modulate spontaneous HIV-1 disease progression by suppressing immune activation or inhibiting antiviral T cell immune responses. While effects of classical CD25hiFoxP3+CD4+ regulatory T cells during HIV-1 infection have been analyzed in a series of recent investigations, very little is known about the role of non-classical regulatory T cells that do not express intracellular FoxP3. Here I evaluated two groups of non-classical Treg cells. One is phenotypically identified by the surface expression of HLA-G, an HLA class Ib molecule. The other Treg cell population is characterized by the surface expression of latency-associated peptide (LAP), a membrane-bound form of TGF-beta. Both HLA-G and LAP-expressing T cells are present in small proportions in peripheral blood of healthy individuals.
520 $a I performed a systematic study on the phenotypic and functional profile of HLA-G- and LAP- expressing regulatory T (Treg) cells in patients with different stages of HIV-1 infection. I found that HLA-G-expressing Treg cells were highly susceptible to HIV-1 infection, and were significantly reduced in individuals with progressive HIV-1 disease courses. Moreover, the proportion of HLA-G + CD4 and CD8 T cells was positively correlated with CD4 T cell count and inversely correlated with markers of HIV-1 associated immune activation. Mechanistically, this correlation corresponded to a substantially increased ability of HLA-G+ Treg cells to inhibit bystander immune activation, while only minimally affecting functional properties of HIV-1-specific T cells. In contrast, no significant change in LAP+ Treg cell frequencies was found in progressive HIV-1 infection, and these frequencies were not correlated with immune activation. This observation was consistent with functional analysis, which indicated that LAP+ Treg cells did not suppress bystander activation. These investigations indicate an important role of HLA-G+ Treg cells for balancing bystander immune activation and anti-viral immune activity in HIV-1 infection, and suggest that the loss of these cells during advanced HIV-1 infection may contribute to immune dysregulation and HIV-1 disease progression. In the meantime, LAP+ Treg cells do not appear to play an important role in determining HIV-1 disease outcome.
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