کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5918333 | 1163858 | 2008 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Human homologues of a Borrelia T cell epitope associated with antibiotic-refractory Lyme arthritis
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Human homologues of a Borrelia T cell epitope associated with antibiotic-refractory Lyme arthritis Human homologues of a Borrelia T cell epitope associated with antibiotic-refractory Lyme arthritis](/preview/png/5918333.png)
چکیده انگلیسی
Antibiotic-refractory Lyme arthritis, which may result from infection-induced autoimmunity, is associated with HLA-DR molecules that bind an epitope of Borrelia burgdorferi (Bb) outer-surface protein A (OspA165-173) and with T cell reactivity with this epitope. One potential mechanism to explain these associations is molecular mimicry between OspA165-173 and a self-peptide. Here, we searched the published human genome for peptides with sequence homology with OspA165-173. The two peptides identified with the greatest sequence homology with the OspA epitope were MAWD-BP276-288, which had identity at eight of the nine core amino acid residues, and T-span758-70, which had identity at six residues. MAWD-BP mRNA was expressed by synoviocytes, while T-span7 mRNA was not. However, neither peptide bound all of the HLA-DR molecules associated with antibiotic-refractory Lyme arthritis. Among 11 patients, 9 had T cell reactivity with OspA161-170, 6 had responses to MAWD-BP276-288, and 3 had reactivity with T-span758-70, but reactivity with the self-peptides was lower than that induced by the spirochetal epitope. Thus, there remains an association between OspA165-173 and antibiotic-refractory Lyme arthritis, and infection-induced autoimmunity is an attractive hypothesis to explain this outcome. However, molecular mimicry due to sequence homology between OspA165-173 and a human peptide seems unlikely to be the critical mechanism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 45, Issue 1, January 2008, Pages 180-189
Journal: Molecular Immunology - Volume 45, Issue 1, January 2008, Pages 180-189
نویسندگان
Elise E. Drouin, Lisa Glickstein, William W. Kwok, Gerald T. Nepom, Allen C. Steere,