Innate and Cell-mediated Immune Responses to Cryptosporidium parvum
This chapter focuses on the innate and cell-mediated immune mechanisms associated with the resistance to and resolution of a Cryptosporidium parvum infection. The results presented in this chapter indicate that both innate and parasite specific-cell-mediated immune responses are involved in immunity...
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Published in | Advances in Parasitology Vol. 40; pp. 87 - 119 |
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Main Author | |
Format | Book Chapter Journal Article |
Language | English |
Published |
England
Elsevier Science & Technology
1998
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Subjects | |
Online Access | Get full text |
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Summary: | This chapter focuses on the innate and cell-mediated immune mechanisms associated with the resistance to and resolution of a Cryptosporidium parvum infection. The results presented in this chapter indicate that both innate and parasite specific-cell-mediated immune responses are involved in immunity to cryptosporidiosis. However, most of the specific components of these responses have not been identified completely. There is a general consensus in the literature to support a role for inteferon-γ (IFNγ) in the initial resistance to C. parvum. However, the mechanism by which IFNγ imparts resistance is unclear. There is also general agreement that CD4+ T cells are important in the resolution of both acute and chronic cryptosporidiosis. Again, the effector mechanism by which these cells eliminate C. parvum from the gastrointestinal tract remains to be determined. There is also some agreement on the IFNγ-mediated control or resolution of cryptosporidiosis. However, the extent to which this cytokine is involved in the actual resolution of infection has been debated. Less extensive studies investigating the participation of other cells and cytokines in the innate and cell-mediated immune responses to C. parvum are also discussed in the chapter. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISBN: | 9780120317400 0120317400 |
ISSN: | 0065-308X 2163-6079 |
DOI: | 10.1016/S0065-308X(08)60118-9 |