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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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Expression of HLA-DR, CD1a, CD86, CD83 on cell surface of antigen-treated DC. G1, antigen-untreated group; G2, inactivated SV40-treated group; G3, infective SV40-treated group. (A) Expression of HLADR on rhesus macaque DC. (B) Expression of CD1a on rhesus ma caque DC. (C) Expression of CD86 on rhesus macaque DC. (D) Expression of CD83 on rhesus macaque DC.
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Figure 3: Expression of HLA-DR, CD1a, CD86, CD83 on cell surface of antigen-treated DC. G1, antigen-untreated group; G2, inactivated SV40-treated group; G3, infective SV40-treated group. (A) Expression of HLADR on rhesus macaque DC. (B) Expression of CD1a on rhesus ma caque DC. (C) Expression of CD86 on rhesus macaque DC. (D) Expression of CD83 on rhesus macaque DC.

Mentions: The expression of HLA-DR, CD1a, CD86, CD83 on cell surface of DC that had been released from CFU in antigen-untreated group, inactivated SV40-treated group, infective SV40-treated group at day 3, 6, 9 of culture were analyzed by flow cytometry. The results showed that, after three days of culture, rhIL-4 cannot significantly elevate the expression of the above molecules except for HLA-DR (Figure 3), and the inactivated SV40 antigen can obviously increase the expression of HLA-DR, CD86 and CD83 (Figure 3A, C, D), while infective SV40, in contrast, can suppress the expression of HLA-DR, CD86 and CD83. The expression of CD1a on DC remained unchanged all the time during the entire study (Figure 3B)


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)

Expression of HLA-DR, CD1a, CD86, CD83 on cell surface of antigen-treated DC. G1, antigen-untreated group; G2, inactivated SV40-treated group; G3, infective SV40-treated group. (A) Expression of HLADR on rhesus macaque DC. (B) Expression of CD1a on rhesus ma caque DC. (C) Expression of CD86 on rhesus macaque DC. (D) Expression of CD83 on rhesus macaque DC.
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Related In: Results  -  Collection

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

Figure 3: Expression of HLA-DR, CD1a, CD86, CD83 on cell surface of antigen-treated DC. G1, antigen-untreated group; G2, inactivated SV40-treated group; G3, infective SV40-treated group. (A) Expression of HLADR on rhesus macaque DC. (B) Expression of CD1a on rhesus ma caque DC. (C) Expression of CD86 on rhesus macaque DC. (D) Expression of CD83 on rhesus macaque DC.
Mentions: The expression of HLA-DR, CD1a, CD86, CD83 on cell surface of DC that had been released from CFU in antigen-untreated group, inactivated SV40-treated group, infective SV40-treated group at day 3, 6, 9 of culture were analyzed by flow cytometry. The results showed that, after three days of culture, rhIL-4 cannot significantly elevate the expression of the above molecules except for HLA-DR (Figure 3), and the inactivated SV40 antigen can obviously increase the expression of HLA-DR, CD86 and CD83 (Figure 3A, C, D), while infective SV40, in contrast, can suppress the expression of HLA-DR, CD86 and CD83. The expression of CD1a on DC remained unchanged all the time during the entire study (Figure 3B)

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