Therefore, a possible concept for lymphocyte depletion during CSFV Tubacin infection might be an aberrant triggering of lymphocytes by an imbalance of virus-induced immune factors or by a viral superantigen. Tregs can suppress immune responses through the production of immunosuppressive cytokines such as TGF-b and IL-10. Anti-inflammatory cytokines such as TGF-b and IL-10 specifically inhibit the release of TNF and other proinflammatory mediators. We found that APS had no effect on TGF-b mRNA expression, but increased IL-10 mRNA expression in PBMCs infected with PRRSV or CSFV. It may be a multistep process in which increased IL-10 initially induces the suppressive environment that may prevent the induction of IL-2 and TNF-a. Interleukin-10 is identified as one of the postulate mechanisms for immunomodulation, both systemically and locally, during an early stage of PRRSV infection. Recent data suggest that the prevalence of IL-10 responses to PRRSV was higher in vaccinated animals than in naı¨ve pigs. On the other hand, the increased IL-10 production during persistent viral infection induces T-cell inactivation and results in the prevention of viral clearance. The synthesis and release of proinflammatory cytokines often represent changes in immune responses during the course of CSF, and TNF-a may be one of the most important proinflammatory mediators in the pathogenesis of the disease. An infection of monocytes by CSFV could induce TNF-a secretion. We showed that primed porcine PBMCs could produce TNF-a in response to PRRSV or CSFV. Notably, TNF-a production was higher in PBMCs infected by PRRSV than by CSFV. It has been shown that TNF-a exerts a strong inhibitory effect on the transcription of the CD28 gene. This may be an explanation for the increased CD28 mRNA expression in PBMCs exposed to CSFV, but not in PBMCs exposed to PRRSV. IFN-c has been thought to play a crucial role against infectious viruses. There is a positive correlation between IFN-c responses induced by vaccination and resistance to the abortifacient effects of PRRSV and the addition of IFN-c inhibited PRRSV replication in macrophages. Previous studies have shown that PRRSV infection failed to elicit any significant inflammatory cytokine expression as an initial response. The production of IFN-c in supernatant was not detected in our study. Although the significance of a relatively low IFN-c response during PRRSV infection relating to protective immunity is unknown, this may allow for the establishment of persistent infection of PRRSV in pigs. In conclusion, the present data indicated that APS alone upregulated IL-2 and TGF-b mRNA expression in PBMCs. The addition of APS to PBMCs infected with PRRSV or CSFV had no effect on TGF-b mRNA expression, downregulated the expression of mRNA for CD28, CTLA-4 and IL-2, but promoted IL-10 mRNA expression. Thus, we suggested that APS had immunomodulatory effects on cells exposed to PRRSV or CSFV. It might be that APS via different mechanisms affects the activities of immune cells during either PRRSV or CSFV infection. This possibility warrants further studies to evaluate whether APS would be an effective adjuvant in vaccines against PRRSV or CSFV. Collagen undergoes several post-translational modifications before formation of a right-handed triple helix in the endoplasmic reticulum.