Fine epitope mapping within the pathogenic thyroglobulin peptide 2340–2359: minimal epitopes retaining antigenicity across various MHC haplotypes are not necessarily immunogenic

Hatzioannou, Aikaterini; Alevizaki, Maria; Carayanniotis, George; Lymberi, Peggy

doi:10.1111/j.1365-2567.2011.03538.x

Cited by 1 publication

(3 citation statements)

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“…In this regard, previous work from our laboratory has shown that while the hTg peptide p2340 elicits EAT in both HR and LR mice, a minimal 9mer epitope within this peptide sequence (aa 2344-2352) was immunopathogenic only in HR strains. 23 The failure of p2208-primed or Tg-primed LNCs to proliferate in vitro in the presence of Tg or peptide, respectively, supports a cryptic role of this peptide in both C57BL/6 and SJL/J hosts. Such a finding is in agreement with several studies in the EAT field that have failed to identify a dominant epitope in Tg.…”

Section: Discussionmentioning

confidence: 90%

“…In the present study, we have not examined whether the pathogenicity of the 20mer p2208 in both H‐2 b and H‐2 s mice can be attributed to recognition of the same minimal epitope within p2208 and the potential role flanking residues might play in the recognition process. In this regard, previous work from our laboratory has shown that while the hTg peptide p2340 elicits EAT in both HR and LR mice, a minimal 9mer epitope within this peptide sequence (aa 2344–2352) was immunopathogenic only in HR strains …”

Section: Discussionmentioning

confidence: 92%

“…In this study, we continued the search to identify pathogenic Tg peptides in LR hosts by assessing the presence of LR and HR MHC class II‐binding motifs in 48 20mer peptides spanning the C‐terminal end of Tg (aa 2172–2749), which had attracted our interest in our previous studies . The peptide p2208 (aa 2208–2227) met our criteria and was subsequently analysed in terms of its T‐cell and B‐cell immunogenicity, as well as the ability to induce EAT in LR and HR mouse strains.…”

Section: Introductionmentioning

confidence: 99%

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A novel pathogenic peptide of thyroglobulin (2208–2227) induces autoreactive T‐cell and B‐cell responses in both high and low responder mouse strains

2014

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Summary Experimental autoimmune thyroiditis (EAT) is commonly induced by thyroglobulin (Tg) or Tg peptides in mice genetically susceptible to thyroiditis. In the present study, we investigated the immunogenic and pathogenic potential of a novel 20mer human Tg peptide, p2208 (amino acids 2208–2227), in mouse strains classified as low (LR) or high (HR) responders in EAT. The peptide was selected for its content in overlapping binding motifs for MHC class II products, associated with either resistance (Ab), or susceptibility (As, Ek) to EAT. We therefore immunized LR BALB/c (H‐2d) and C57BL/6 (H‐2b) strains, as well as HR CBA/J (H‐2k) and SJL/J (H‐2s) mice with 100 nmol of p2208 in adjuvant and collected their sera, lymph nodes and thyroid glands for further analysis. The p2208 peptide was found to contain B‐cell and cryptic T‐cell epitope(s) in two of the four strains examined, one LR and one HR. Specifically, it elicited direct EAT in C57BL/6 mice (two of seven mice, infiltration index 1–3), as well as in SJL/J mice (two of six mice, infiltration index 1–2). Such an EAT model could provide insights into the immunoregulatory cascades taking place in resistant hosts.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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