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Human T-cell leukemia virus type-I Tax induces the expression of CD83 on T cells.

Tanaka Y, Mizuguchi M, Takahashi Y, Fujii H, Tanaka R, Fukushima T, Tomoyose T, Ansari AA, Nakamura M - Retrovirology (2015)

Bottom Line: We found that CD83 was expressed selectively on Tax1-expressing human CD4(+) T cells in short-term cultured peripheral blood mononuclear cells (PBMCs) isolated from HTLV-I(+) donors, including ATL patients and HTLV-I carriers.The CD83 promoter was activated by Tax1 in an NF-κB-dependent manner.Our results suggest that HTLV-I induces CD83 expression on T cells via Tax1 -mediated NF-κB activation, which may promote HTLV-I infection in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara-cho, Okinawa, 903-0215, Japan. yuetsu@s4.dion.ne.jp.

ABSTRACT

Background: CD83, a cell surface glycoprotein that is stably expressed on mature dendritic cells, can be transiently induced on other hematopoietic cell lineages upon cell activation. In contrast to the membrane form of CD83, soluble CD83 appears to be immunosuppressive. In an analysis of the phenotype of leukemic CD4(+) T cells from patients with adult T-cell leukemia (ATL), we found that a number of primary CD4(+) T cells became positive for cell surface CD83 after short-term culture, and that most of these CD83(+) CD4(+) T cells were positive for human T-cell leukemia virus type-I (HTLV-I) Tax (Tax1). We hypothesized that Tax1 is involved in the induction of CD83.

Result: We found that CD83 was expressed selectively on Tax1-expressing human CD4(+) T cells in short-term cultured peripheral blood mononuclear cells (PBMCs) isolated from HTLV-I(+) donors, including ATL patients and HTLV-I carriers. HTLV-I-infected T cell lines expressing Tax1 also expressed cell surface CD83 and released soluble CD83. CD83 can be expressed in the JPX-9 cell line by cadmium-mediated Tax1 induction and in Jurkat cells or PBMCs by Tax1 introduction via infection with a recombinant adenovirus carrying the Tax1 gene. The CD83 promoter was activated by Tax1 in an NF-κB-dependent manner. Based on a previous report showing soluble CD83-mediated prostaglandin E2 (PGE2) production from human monocytes in vitro, we tested if PGE2 affected HTLV-I propagation, and found that PGE2 strongly stimulated expression of Tax1 and viral structural molecules.

Conclusions: Our results suggest that HTLV-I induces CD83 expression on T cells via Tax1 -mediated NF-κB activation, which may promote HTLV-I infection in vivo.

No MeSH data available.


Related in: MedlinePlus

Induction of CD83 expression by Tax1. a CD83 and Tax1 co-expression (Panel 1), OX40 and Tax1 co-expression (Panel 2), and OX40 and CD83 co-expression (Panel 3) in JPX-9 cells were examined by FCM. Cells were cultured either in medium alone (upper columns) or in the presence of 10 μM CdCl2 (lower columns) for 3 days. b PBMCs and Jurkat cells were infected with recombinant Tax1 adenovirus (Ad-Tax1) or wild-type virus (Ad-Con), cultured for 48 h and harvested for mRNA isolation. The levels of CD83 mRNA were measured by quantitative PCR with specific primers indicated in the Methods section. The results are shown as the mean ± SE after normalization against 18S rRNA.
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Fig5: Induction of CD83 expression by Tax1. a CD83 and Tax1 co-expression (Panel 1), OX40 and Tax1 co-expression (Panel 2), and OX40 and CD83 co-expression (Panel 3) in JPX-9 cells were examined by FCM. Cells were cultured either in medium alone (upper columns) or in the presence of 10 μM CdCl2 (lower columns) for 3 days. b PBMCs and Jurkat cells were infected with recombinant Tax1 adenovirus (Ad-Tax1) or wild-type virus (Ad-Con), cultured for 48 h and harvested for mRNA isolation. The levels of CD83 mRNA were measured by quantitative PCR with specific primers indicated in the Methods section. The results are shown as the mean ± SE after normalization against 18S rRNA.

Mentions: The potential ability of Tax1 to induce CD83 expression was examined using the Tax1-inducible human T cell line JPX-9. Incubation with CdCl2, which is required for Tax1 expression, induced apparent cell surface CD83 expression on JPX-9 cells (Figure 5a). Importantly, CD83 expression was predominantly restricted to Tax1+ cells. The majority of Tax1+ cells also expressed OX40, a representative protein that is also induced by Tax1 on T cells [34].Figure 5


Human T-cell leukemia virus type-I Tax induces the expression of CD83 on T cells.

Tanaka Y, Mizuguchi M, Takahashi Y, Fujii H, Tanaka R, Fukushima T, Tomoyose T, Ansari AA, Nakamura M - Retrovirology (2015)

Induction of CD83 expression by Tax1. a CD83 and Tax1 co-expression (Panel 1), OX40 and Tax1 co-expression (Panel 2), and OX40 and CD83 co-expression (Panel 3) in JPX-9 cells were examined by FCM. Cells were cultured either in medium alone (upper columns) or in the presence of 10 μM CdCl2 (lower columns) for 3 days. b PBMCs and Jurkat cells were infected with recombinant Tax1 adenovirus (Ad-Tax1) or wild-type virus (Ad-Con), cultured for 48 h and harvested for mRNA isolation. The levels of CD83 mRNA were measured by quantitative PCR with specific primers indicated in the Methods section. The results are shown as the mean ± SE after normalization against 18S rRNA.
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4487981&req=5

Fig5: Induction of CD83 expression by Tax1. a CD83 and Tax1 co-expression (Panel 1), OX40 and Tax1 co-expression (Panel 2), and OX40 and CD83 co-expression (Panel 3) in JPX-9 cells were examined by FCM. Cells were cultured either in medium alone (upper columns) or in the presence of 10 μM CdCl2 (lower columns) for 3 days. b PBMCs and Jurkat cells were infected with recombinant Tax1 adenovirus (Ad-Tax1) or wild-type virus (Ad-Con), cultured for 48 h and harvested for mRNA isolation. The levels of CD83 mRNA were measured by quantitative PCR with specific primers indicated in the Methods section. The results are shown as the mean ± SE after normalization against 18S rRNA.
Mentions: The potential ability of Tax1 to induce CD83 expression was examined using the Tax1-inducible human T cell line JPX-9. Incubation with CdCl2, which is required for Tax1 expression, induced apparent cell surface CD83 expression on JPX-9 cells (Figure 5a). Importantly, CD83 expression was predominantly restricted to Tax1+ cells. The majority of Tax1+ cells also expressed OX40, a representative protein that is also induced by Tax1 on T cells [34].Figure 5

Bottom Line: We found that CD83 was expressed selectively on Tax1-expressing human CD4(+) T cells in short-term cultured peripheral blood mononuclear cells (PBMCs) isolated from HTLV-I(+) donors, including ATL patients and HTLV-I carriers.The CD83 promoter was activated by Tax1 in an NF-κB-dependent manner.Our results suggest that HTLV-I induces CD83 expression on T cells via Tax1 -mediated NF-κB activation, which may promote HTLV-I infection in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara-cho, Okinawa, 903-0215, Japan. yuetsu@s4.dion.ne.jp.

ABSTRACT

Background: CD83, a cell surface glycoprotein that is stably expressed on mature dendritic cells, can be transiently induced on other hematopoietic cell lineages upon cell activation. In contrast to the membrane form of CD83, soluble CD83 appears to be immunosuppressive. In an analysis of the phenotype of leukemic CD4(+) T cells from patients with adult T-cell leukemia (ATL), we found that a number of primary CD4(+) T cells became positive for cell surface CD83 after short-term culture, and that most of these CD83(+) CD4(+) T cells were positive for human T-cell leukemia virus type-I (HTLV-I) Tax (Tax1). We hypothesized that Tax1 is involved in the induction of CD83.

Result: We found that CD83 was expressed selectively on Tax1-expressing human CD4(+) T cells in short-term cultured peripheral blood mononuclear cells (PBMCs) isolated from HTLV-I(+) donors, including ATL patients and HTLV-I carriers. HTLV-I-infected T cell lines expressing Tax1 also expressed cell surface CD83 and released soluble CD83. CD83 can be expressed in the JPX-9 cell line by cadmium-mediated Tax1 induction and in Jurkat cells or PBMCs by Tax1 introduction via infection with a recombinant adenovirus carrying the Tax1 gene. The CD83 promoter was activated by Tax1 in an NF-κB-dependent manner. Based on a previous report showing soluble CD83-mediated prostaglandin E2 (PGE2) production from human monocytes in vitro, we tested if PGE2 affected HTLV-I propagation, and found that PGE2 strongly stimulated expression of Tax1 and viral structural molecules.

Conclusions: Our results suggest that HTLV-I induces CD83 expression on T cells via Tax1 -mediated NF-κB activation, which may promote HTLV-I infection in vivo.

No MeSH data available.


Related in: MedlinePlus