Reader Comments
Post a new comment on this article
Post Your Discussion Comment
Please follow our guidelines for comments and review our competing interests policy. Comments that do not conform to our guidelines will be promptly removed and the user account disabled. The following must be avoided:
- Remarks that could be interpreted as allegations of misconduct
- Unsupported assertions or statements
- Inflammatory or insulting language
Thank You!
Thank you for taking the time to flag this posting; we review flagged postings on a regular basis.
closeAuthor Summary
Posted by sandrammuxel on 25 Jul 2011 at 14:02 GMT
The asexual blood-stages of Plasmodium spp. are responsible for the clinical symptoms of malaria. CD4+ T cells are implicated in the development of both disease pathogenesis and protective immunity. Herein, we examined in detail the behaviour of splenic CD4+ T cells during blood-stage Plasmodium chabaudi malaria. The CD4+ T cell response to infection develops in two consecutive phases concomitant with the acute and chronic parasitaemias. The early phase of the response is intense and short-lasting, rapidly providing large amounts of proinflammatory cytokines and helping B cells to secrete polyclonal immunoglobulin. The abrupt elimination of a great proportion of CD4+ T cells, together with a period of CD4+ T cell unresponsiveness, gives opportunity to the development of acquired immunity. During the late phase of the response, a large pool of CD4+ T cells is generated with the ability to promptly proliferate and produce IFN-γ when stimulated with parasites. These cells also cooperate with B cells for production of parasite-specific antibodies. Conventional CD4+ T cells are the main protagonists of this response from the onset of the disease, acting in parallel with non-conventional CD4+ T cells as a bridge between the innate and acquired immunity.