Variability and exclusion in host and parasite: epigenetic regulation of Ig and var expression.
The immune system generates highly diverse AgRs of different specificities from a pool of designated genomic loci, each containing large arrays of genes. Ultimately, each B or T cell expresses a receptor of a single type on its surface. Immune evasion by the malaria parasite Plasmodium falciparum is mediated by the mutually exclusive expression of a single member of the var family of genes, which encodes variant surface Ags. In this review, we discuss the similarities as well as the unique characteristics of the epigenetic mechanisms involved in the establishment of mutually exclusive expression in the immune and parasite systems.
Fraenkel
Shira
S
Department of Experimental Medicine and Cancer Research, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel.
Bergman
Yehudit
Y
D000818:Animals; D000940:Antigenic Variation / Q000235:genetics*; D044127:Epigenesis, Genetic; D015322:Gene Rearrangement, B-Lymphocyte; D007136:Immunoglobulins / Q000235:genetics; D016778:Malaria, Falciparum / Q000235:genetics / Q000276:immunology*; D051379:Mice; D010963:Plasmodium falciparum / Q000235:genetics / Q000472:pathogenicity*; D015800:Protozoan Proteins / Q000235:genetics*
D007136:Immunoglobulins; D015800:Protozoan Proteins; C085731:erythrocyte membrane protein 1, Plasmodium falciparum