Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.53 (sialidase)
 2,694 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polyclonal lymphocyte activation and hypergammaglobulinemia characterize the acute phase of Chagas' disease, a debilitating condition caused by Trypanosoma cruzi. Such pathogenic hyper-reactivities not only compromise specific host defense against the pathogen, but may also contribute to infection-induced chronic autoimmune responses. Recent studies showed that T. cruzi trans-sialidase (TS) directly stimulates the polyclonal proliferation and Ig secretion of normal murine B cells in a T-independent, Bruton's tyrosine kinase (Btk)-dependent manner. Related to this observation, we now show that parasite-derived and recombinant TS potentiate the proliferation and cytokine secretion of normal T cells triggered by antigen-specific and non-specific stimuli. TS potentiates T cell activation through stimulating B cells and macrophages, independent of CD40/CD40L and CD43 pathways. In contrast, optimal TS potentiation requires interleukin-6 (IL-6) and Btk, as it is significantly reduced in splenocytes from IL-6-/- and Btk-defective Xid mice. The results suggest that TS, directly and indirectly, activates both antigen-presenting cell and T cell compartments, and that TS-induced IL-6 may further amplify such activation. These observations open up the possibility that TS drives the polyclonal lymphocyte activation in acute T. cruzi infection, a phenomenon contributing to the pathogenesis of Chagas' disease.
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PMID:Trypanosoma cruzi trans-sialidase potentiates T cell activation through antigen-presenting cells: role of IL-6 and Bruton's tyrosine kinase. 1146 7