ترجمه مقاله نقش ضروری ارتباطات 6G با چشم انداز صنعت 4.0
- مبلغ: ۸۶,۰۰۰ تومان
ترجمه مقاله پایداری توسعه شهری، تعدیل ساختار صنعتی و کارایی کاربری زمین
- مبلغ: ۹۱,۰۰۰ تومان
Abstract
Toxoplasma gondii is a protozoan parasite that infects humans and animals via congenital or postnatal routes. During parasite infection, IL-10-producing Bregs are stimulated as part of the parasite-induced host immune responses that favor infection. In this study, we investigated whether T. gondii infection induces immune regulatory cells including IL-10-producing CD1dhighCD5þ regulatory B cells (Bregs) and whether Breg induction is critical for the development of chronic infection of T. gondii. Furthermore, B cell-deficient (μMT) mice revealed that the IL-10-producing B cells might be associated with the development of chronic T. gondii infection. To better understand the mechanism underlying the accumulation of IL-10-producing B cells upon T. gondii infection, we determined the effect of products released by T. gondii on the induction and differentiation of IL-10-producing B cells during the acute stage of infection using transgenic green fluorescent protein (GFP)-expressing T. gondii strain. We demonstrated that products secreted at the stage of cell lysis by fully replicated tachyzoites induced the differentiation of naive B cells to IL-10-producing Bregs. Our results indicated that the downregulation of the immune response via Bregs during T. gondii infection is related to cyst formation in the host brain and to the establishment of chronic infection.
4. Discussion
The development of chronic parasite infection is believed to result from the suppression of host immune responses. As T. gondii infection is usually chronic, it is likely that the parasite modulates the host immune system to prevent its own destruction. The findings in this study indicated that the induction of IL-10-producing Bregs in response to T. gondii infection may play an important role in the development of chronic infection as a part of the parasite evasion strategy against host immune mechanisms (Fig. 5). We observed that a significant increase of the IL-10-producing CD1highCD5þCD19þ Breg subset during T. gondii infection was accompanied by increased cyst formation in the brain, which is a characteristic feature of chronic T. gondii infection (Figs. 2A and B).