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<jats:p>T cells are central to immunity in malaria. CD4<jats:sup>+</jats:sup> helper T cells favour the generation of high-affinity antibodies that are effective against blood stages and they are necessary to establish immunological memory. The intrahepatic stage of infection can be eliminated by specific CD8<jats:sup>+</jats:sup> cytotoxic T cells (CTL). Cytokines secreted by CD4<jats:sup>+</jats:sup> T cells may also contribute to liver stage immunity. Evolution has selected varied mechanisms in pathogens to avoid recognition by T cells. T cells recognize foreign epitopes as complexes with host major histocompatibility (MHC) molecules. Thus, a simple form of evasion is to mutate amino acid residues which allow binding to an MHC allele. Recently, more sophisticated forms of polymorphic evasion have been described. In <jats:italic>altered peptide ligand</jats:italic> (<jats:italic>APL</jats:italic>) <jats:italic>antagonism</jats:italic>, the concurrent presentation of particular closely related epitope variants can prevent memory T cell effector functions such as cytotoxicity, lymphokine production and proliferation. In <jats:italic>immune interference</jats:italic>, the effect of the concurrent presentation of such related epitope variants can go a step further and prevent the induction of memory T cells from naive precursors. The analysis of immune responses to a protein of <jats:italic>P. falciparum</jats:italic>, the circumsporozoite protein (CSP), indicates that the malaria parasite may utilize these evasion strategies.</jats:p>

Original publication

DOI

10.1017/s0031182097002035

Type

Journal article

Journal

Parasitology

Publisher

Cambridge University Press (CUP)

Publication Date

12/1997

Volume

115

Pages

55 - 66