Induction of CD4+ and CD8+Bordetella pertussis Toxin Subunit S1 Specific T Cells by Immunization with Synthetic Peptides

Fagerberg, Jan; Askelöf, Per; Wigzell, Hans; Mellstedt, Håkan

doi:10.1006/cimm.1999.1548

Cited by 1 publication

(1 citation statement)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of studies have identified associations between MHC class II (MHC II) with disease susceptibility, resistance or severity caused by M. tuberculosis and P. falciparum . In addition, there are reports of MHC II‐restricted immune response to vaccination with peptides derived from B. pertussis [pertussis toxin subunit ] as well as increased expression of MHC II DR loci in H. pylori ‐positive gastritis patients .…”

Section: Methodsmentioning

confidence: 99%

A limit to the divergent allele advantage model supported by variable pathogen recognition across HLA‐DRB1 allele lineages

2015

View full text Add to dashboard Cite

Genetic diversity in human leukocyte antigen (HLA) molecules is thought to have arisen from the co‐evolution between host and pathogen and maintained by balancing selection. Heterozygote advantage is a common proposed scenario for maintaining high levels of diversity in HLA genes, and extending from this, the divergent allele advantage (DAA) model suggests that individuals with more divergent HLA alleles bind and recognize a wider array of antigens. While the DAA model seems biologically suitable for driving HLA diversity, there is likely an upper threshold to the amount of sequence divergence. We used peptide‐binding and pathogen‐recognition capacity of DRB1 alleles as a model to further explore the DAA model; within the DRB1 locus, we examined binding predictions based on two distinct phylogenetic groups (denoted group A and B) previously identified based on non‐peptide‐binding region (PBR) nucleotide sequences. Predictions in this study support that group A allele and group B allele lineages have contrasting binding/recognition capacity, with only the latter supporting the DAA model. Furthermore, computer simulations revealed an inconsistency in the DAA model alone with observed extent of polymorphisms, supporting that the DAA model could only work effectively in combination with other mechanisms. Overall, we support that the mechanisms driving HLA diversity are non‐exclusive. By investigating the relationships among HLA alleles, and pathogens recognized, we can provide further insights into the mechanisms on how humans have adapted to infectious diseases over time.

show abstract

Section: Methodsmentioning

confidence: 99%