English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Toxoplasma gondii  is an obligatory intracellular parasite that causes a common infection in many warm-blooded animals. During infection, the host’s immune system plays an important role in confining the dissemination of the parasites in the hosts. T cell immunoglobulin- and mucin domain–containing molecule 3 (Tim-3) has been characterized as an important regulator in cell-mediated immune responses in various infections. Here, we compared Tim-3 expression on splenic and circulatory T, B cells and a few cytokines in the sera of mice infected with the more virulent type I (RH) vs. the low virulent type II (ME49) strain. Tim-3 expression on the splenic and circulatory T cells of mice infected with  T. gondii  (RH strain) was higher than that in mice infected with  T. gondii  (ME49 strain).  T. gondii  infection reduced the proportion of splenic helper T cells (Th) and cytotoxic T cells (Tc) and increased Tim-3 expression. Further, serum levels of interleukin (IL)-2, interferon γ, tumor necrosis factor (TNF)-α, IL-12p70, IL-22, IL-17A, and IL-5 increased significantly after infection. Mice infected with  T. gondii  (ME49 strain) showed higher levels of TNF-α, IL-17A, IL-12p70, and IL-22 than that infected by the RH strain. Our study revealed that  T. gondii  strains may have their inherent ability in triggering different host immune responses, which may explain the clinical variation in diseases severity after infection.

Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice