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Simian virus 40 inhibits differentiation and maturation of rhesus macaque DC-SIGN(+) dendritic cells.

Changyong C, Sun M, Li H, Brockmeyer N, Wu NP - Eur. J. Med. Res. (2010)

Bottom Line: Dendritic cells (DC) are the initiators and modulators of the immune responses.Results showed that SV40 can down-regulate the expression of CD83 and CD86 on DC and impair DC-induced activation of T cell proliferation.These findings suggest that SV40 might also cause immune suppression by influencing differentiation and maturation of DC.

View Article: PubMed Central - HTML - PubMed

Affiliation: The State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou, PR China.

ABSTRACT
Dendritic cells (DC) are the initiators and modulators of the immune responses. Some species of pathogenic microorganisms have developed immune evasion strategies by controlling antigen presentation function of DC. Simian virus 40 (SV40) is a DNA tumor virus of rhesus monkey origin. It can induce cell transformation and tumorigenesis in many vertebrate species, but often causes no visible effects and persists as a latent infection in rhesus monkeys under natural conditions. To investigate the interaction between SV40 and rhesus monkey DC, rhesus monkey peripheral blood monocyte-derived DC were induced using recombinant human Interleukin-4 (rhIL-4) and infective SV40, the phenotype and function of DC-specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN)(+) DC were analyzed by flow cytometry (FCM) and mixed lymphocyte reaction (MLR). Results showed that SV40 can down-regulate the expression of CD83 and CD86 on DC and impair DC-induced activation of T cell proliferation. These findings suggest that SV40 might also cause immune suppression by influencing differentiation and maturation of DC.

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Cell proliferation effect of auto T cell activated by DC in mixed lymphocyte reaction. cpm, counts per minute; G2, inactivated SV40-treated group; G3, infective SV40-treated group.
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Figure 4: Cell proliferation effect of auto T cell activated by DC in mixed lymphocyte reaction. cpm, counts per minute; G2, inactivated SV40-treated group; G3, infective SV40-treated group.

Mentions: In this study, the phenotype and function of infective SV40-treated peripheral blood monocytes derived DC were analyzed. The results showed that the phenotype and function of inactivated SV40-treated DC and infective SV40-treated DC are rather different. The expression levels of major histocompatibility complex (MHC) class II molecules, CD86 and CD83 of infective SV40-treated DC on day 6, 9 of culture were lower than those of inactivated SV40-treated DC (Figure 3A, C, D). T cell proliferation activity stimulated by infective SV40-treated DC was also lower than that stimulated by inactivated SV40-treated DC (Figure 4). MHC class II molecule of DC is related to antigen processing and presentation of exogenous antigen. CD86 is an important costimulatory molecule for the priming of naive T cells. CD83 is one of the best markers for mature dendritic cells. Recent studies showed that CD83 expressed on DC plays a costimulatory role in T cell initiation [43]. Although CD209+ DC can uptake infective SV40, the virus infection is not productive. Down-regulation of the expression of MHC class II molecules, CD86 and CD83 on infective SV40-treated DC suggests that infective SV40 can inhibit the differentiation and maturation of rhesus macaque DCSIGN+ dendritic cells and subvert antigen presentation function of DC. Compare with inactivated SV40 antigen, infective SV40 can significantly down-regulate the expression of dendritic cell-derived interleukin-12 and facilitates immunosuppression (Figure 4). These preliminary data suggest that SV40 can manipulate antigen presentation function of DC-SIGN+ DC and initiate immune tolerance.


Simian virus 40 inhibits differentiation and maturation of rhesus macaque DC-SIGN(+) dendritic cells.

Changyong C, Sun M, Li H, Brockmeyer N, Wu NP - Eur. J. Med. Res. (2010)

Cell proliferation effect of auto T cell activated by DC in mixed lymphocyte reaction. cpm, counts per minute; G2, inactivated SV40-treated group; G3, infective SV40-treated group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3351904&req=5

Figure 4: Cell proliferation effect of auto T cell activated by DC in mixed lymphocyte reaction. cpm, counts per minute; G2, inactivated SV40-treated group; G3, infective SV40-treated group.
Mentions: In this study, the phenotype and function of infective SV40-treated peripheral blood monocytes derived DC were analyzed. The results showed that the phenotype and function of inactivated SV40-treated DC and infective SV40-treated DC are rather different. The expression levels of major histocompatibility complex (MHC) class II molecules, CD86 and CD83 of infective SV40-treated DC on day 6, 9 of culture were lower than those of inactivated SV40-treated DC (Figure 3A, C, D). T cell proliferation activity stimulated by infective SV40-treated DC was also lower than that stimulated by inactivated SV40-treated DC (Figure 4). MHC class II molecule of DC is related to antigen processing and presentation of exogenous antigen. CD86 is an important costimulatory molecule for the priming of naive T cells. CD83 is one of the best markers for mature dendritic cells. Recent studies showed that CD83 expressed on DC plays a costimulatory role in T cell initiation [43]. Although CD209+ DC can uptake infective SV40, the virus infection is not productive. Down-regulation of the expression of MHC class II molecules, CD86 and CD83 on infective SV40-treated DC suggests that infective SV40 can inhibit the differentiation and maturation of rhesus macaque DCSIGN+ dendritic cells and subvert antigen presentation function of DC. Compare with inactivated SV40 antigen, infective SV40 can significantly down-regulate the expression of dendritic cell-derived interleukin-12 and facilitates immunosuppression (Figure 4). These preliminary data suggest that SV40 can manipulate antigen presentation function of DC-SIGN+ DC and initiate immune tolerance.

Bottom Line: Dendritic cells (DC) are the initiators and modulators of the immune responses.Results showed that SV40 can down-regulate the expression of CD83 and CD86 on DC and impair DC-induced activation of T cell proliferation.These findings suggest that SV40 might also cause immune suppression by influencing differentiation and maturation of DC.

View Article: PubMed Central - HTML - PubMed

Affiliation: The State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou, PR China.

ABSTRACT
Dendritic cells (DC) are the initiators and modulators of the immune responses. Some species of pathogenic microorganisms have developed immune evasion strategies by controlling antigen presentation function of DC. Simian virus 40 (SV40) is a DNA tumor virus of rhesus monkey origin. It can induce cell transformation and tumorigenesis in many vertebrate species, but often causes no visible effects and persists as a latent infection in rhesus monkeys under natural conditions. To investigate the interaction between SV40 and rhesus monkey DC, rhesus monkey peripheral blood monocyte-derived DC were induced using recombinant human Interleukin-4 (rhIL-4) and infective SV40, the phenotype and function of DC-specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN)(+) DC were analyzed by flow cytometry (FCM) and mixed lymphocyte reaction (MLR). Results showed that SV40 can down-regulate the expression of CD83 and CD86 on DC and impair DC-induced activation of T cell proliferation. These findings suggest that SV40 might also cause immune suppression by influencing differentiation and maturation of DC.

Show MeSH
Related in: MedlinePlus