| Autor: |
Acosta Rodriguez EV; Department of Clinical Biochemistry, School of Chemical Science, National University of Córdoba, Córdoba, Argentina., Zuniga EI, Montes CL, Merino MC, Bermejo DA, Amezcua Vesely MC, Motran CC, Gruppi A |
| Jazyk: |
angličtina |
| Zdroj: |
Scandinavian journal of immunology [Scand J Immunol] 2007 Aug-Sep; Vol. 66 (2-3), pp. 137-42. |
| DOI: |
10.1111/j.1365-3083.2007.01968.x |
| Abstrakt: |
Trypanosoma cruzi, the causative agent of Chagas' disease, may sabotage humoral response by affecting B cells at the different stages of its development. The present review highlights the contributions of our laboratory in understanding how T. cruzi hinders B-cell generation and B-cell expansion limiting host defence and favouring its chronic establishment. We discuss how homoeostatic mechanisms can be triggered to control exacerbated B-cell proliferation that favour T. cruzi infection by eliminating parasite-specific B cells. Specific targeting of evasion mechanisms displayed in T. cruzi infection, as in vivo Fas/FasL blockade or Gal-3 expression inhibition, allowed us to modulate B-cell responses enhancing the anti-parasite humoral immune response. A comprehensive understanding of the biology of the B cell in health and disease is strictly required to devise immunointervention strategies aimed at enhancing protective immune responses during infections. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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