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Toxoplasma Gondii Antigens

Toxoplasma Gondii Antigen Products by Targets

Modulation of innate immunity by secretory proteins ROP5, ROP16 and ROP18Fig. 1 Modulation of innate immunity by secretory proteins ROP5, ROP16 and ROP18 (Y. Zhang, et al. 2019)

Life cycle of T. gondii Fig. 2 Life cycle of T. gondii (Wikipedia, Public Domain)

Toxoplasma gondii (T. gondii) is a parasite that causes the disease toxoplasmosis. It is an obligate intracellular, alveolate parasite that belongs to the family Sarcocystidae, genus Toxoplasma. T.gondii is capable of infecting nearly all the warm-blood animals. However, sexual reproduction of this parasite can only be found in felids such as domestic cats. T. gondii is one of the most common parasites in humans, in developing countries. Serological studies suggest that 30% -50% of the global population were thought to be exposed to T. gondii and may be chronically infected.

T. gondii infections humans through several ways such as eating poorly cooked food that contains cysts, exposure to infected cat feces, and from infected mother to her child during pregnancy. The infection of T. gondii has three forms: acute toxoplasmosis, latent toxoplasmosis and cutaneous toxoplasmosis. More than 50% of the world population is thought to be infected but without any symptoms. Occasionally there may be a few weeks or months of mild flu-like illness. Symptoms may include fever, swollen lymph nodes, headaches, fatigue, muscle aches, etc. T. gondii is also capable of altering the behavior of infected rodents which will increase the rodents' chances of being preyed upon by felids.

The life cycle of T. gondii can be generally summarized into two components: the sexual component and the asexual component. The sexual component can only occurs in felids, wild or domestic cats, meaning that T. gondii can only proceed to the sexual reproduction within their definitive host, cats. While the asexual component can be found in virtually all warm-blooded animal hosts, including humans, cats, birds, rodents.

Three secretory organelles are present in the cytoplasm of T. gondii: microneme, rhoptry, and dense granule, which are known to function in the entry of the parasite and maintain intracellular host-parasite relationships, as unique to the parasites of the phylum Apicomplexa. T. gondii secretes a broad spectrum of proteins, including MICs, ROPs and GRAs. MICs, ROPs and GRAs differ in their localization and their time of release from the cell.

  • MICs MICs localize in the apical end of T. gondii. MICs play a role in motility and adhesion of T. gondii. MIC1, MIC2, MIC4, MIC6 and particularly MIC3 were shown to bind to a broad spectrum of targets, such as adolase, glucose, ICAM-1, lactose, and heparin. Furthermore, secreted MIC2 is crucial for the motility of T. gondii.
  • ROPs ROPs are involved in the formation of the parasitophorous vacuole as evidenced by the localization of ROP2, ROP4, ROP5, ROP7, ROP8, and ROP18 at the parasitophorous vacuolar membrane (PVM). ROP2 has been implicated in the acquisition association of PVM with host’s mitochondria. The association between mitochondria and the PV was shown to be dependent on the host cell type.
  • GRAs In the dense granule, there are 12 GRA proteins (GRA1-GRA14, but GRA11 and 13 are phantom-like) that have been previously identified in T. gondii tachyzoites without sequence homology to each other in addition to 2 isoforms of nucleotide triphosphate hydrolase (NTPase I and II) and 2 protease inhibitors (TgPI 1 and 2). All the GRA proteins are identified as excretory/secretory antigen (ESP). They all contain signal sequences of 25-30 amino acids, except for GRA3 and GRA6, and this would target to the secretory pathway of the parasite.

With years of protein and antigen production experience, professional science teams and stat-of-art platforms, Creative Diagnostics now can provide high-quality T. gondii antigens for academic and industry applications, including T. gondii Rhoptry proteins, T. gondii MIC, T. gondii p30 protein. Welcome to contact us for more details.

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