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As a multicellular parasitic nematode,  Trichinella spiralis  regulates host immune responses by producing a variety of immunomodulatory molecules to escape from host immune attack, but the mechanisms underlying the immune evasion are not well understood. Here, we identified that  T. spiralis  calreticulin ( Ts -CRT), a Ca 2+ -binding protein, facilitated  T. spiralis  immune evasion by interacting with the first component of human classical complement pathway, C1q. In the present study,  Ts -CRT was found to be expressed on the surface of different developmental stages of  T. spiralis  as well as in the secreted products of adult and muscle larval worms. Functional analysis identified that  Ts -CRT was able to bind to human C1q, resulting in the inhibition of C1q-initiated complement classical activation pathway reflected by reduced C4/C3 generation and C1q-dependent lysis of antibody-sensitized sheep erythrocytes. Moreover, recombinant  Ts -CRT (r Ts -CRT) binding to C1q suppressed C1q-induced THP-1-derived macrophages chemotaxis and reduced monocyte–macrophages release of reactive oxygen intermediates (ROIs). Blocking  Ts -CRT on the surface of newborn larvae (NBL) of  T. spiralis  with anti- Ts -CRT antibody increased the C1q-mediated adherence of monocyte–macrophages to larvae and impaired larval infectivity. All of these results suggest that  T. spiralis -expressed  Ts -CRT plays crucial roles in  T. spiralis  immune evasion and survival in host mostly by directly binding to host complement C1q, which not only reduces C1q-mediated activation of classical complement pathway but also inhibits the C1q-induced non-complement activation of macrophages.

Trichinella spiralis Calreticulin Binds Human Complement C1q As an Immune Evasion Strategy