T Cell Receptor Cross-Reactivity between Similar Foreign and Self Peptides Influences Naive Cell Population Size and Autoimmunity

Abstract

Table 1 of this paper published in the January 2015 issue contains several errors. The Derp1 peptide comes from the Der p1 protein of Dermatophagoides pteronyssinus not the Der f1 protein of Dermatophagoides farinae. The sequence of the MOG peptide in the I-A b tetramer used in the study was GWYRSPFSRVV not GWYRSPFSRVVVHLY. The most likely 9 amino acid core register for the OVA2C peptide in the I-A b tetramer used in the study is VHAAHAEIN not AVHAAHAEI, which is the second most likely. The most likely register has a different number of predicted self peptide homologs than the second most likely one, which changed the x axis value for the OVA2C peptide in Figure 4G. However, neither the level of statistical significance of the correlation between the number of self peptide homologs and the number of naive cells specific for foreign peptides shown in Figure 4G nor the conclusion that ''TCR cross-reactivity on self-peptide homologs plays some role in determining the size of MHCII-bound foreign peptide-specific CD4 + T cell populations'' were changed. Thus, none of these errors affect any of the conclusions of the paper. The authors deeply regret these errors and apologize for them. Corrected versions of the table and figure appear here.

Weakly self‐reactive T‐cell clones can homeostatically expand when present at low numbers

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The Case for Absolute Ligand Discrimination: Modeling Information Processing and Decision by Immune T Cells

“…There is a similar disconnect between the dynamics of biological problems at stake (eradicating a fast-replicating fast evolving pathogen vs. generating an adaptive immune response). In particular, recent measurements by the Jenkins and Davis lab [28,51] have beautifully illustrated the number of constraints for a good immune response. Lymphocytes can rapidly proliferate (by factors of 10 3 to 10 6 ) and relax back to low numbers for the memory pool.…”

iVAX: An integrated toolkit for the selection and optimization of antigens and the design of epitope-driven vaccines

“…If TCR-facing residues from a pathogenic epitope are conserved among multiple HLA-binding sequences from the human genome, the pathogenic epitope may activate T cells specific to these human proteins. This may lead to a lack of response due to low precursor T cell frequency, 49 a regulatory response generated by natural Tregs, or a harmful autoimmune response, all of which are unwanted effects in a vaccine. To address these possibilities, we developed JanusMatrix to identify EpiMatrixpredicted epitopes that may activate tolerogenic or auto-reactive effector T cells.…”