کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3342243 1214273 2009 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Autoimmune thyroiditis as an indicator of autoimmune sequelae during cancer immunotherapy
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Autoimmune thyroiditis as an indicator of autoimmune sequelae during cancer immunotherapy
چکیده انگلیسی

Improving cancer immunotherapy by targeting T cell network also triggers autoimmunity. We disrupted regulatory T cell (Treg) function to probe the balance between breast cancer vaccination and autoimmune thyroiditis (EAT) in four models, with particular attention to MHC-associated susceptibility, EAT induction with mouse thyroglobulin (mTg) without adjuvant, and tolerance to Her-2/neu in transgenic mice. 1) In EAT-resistant BALB/c mice, Treg depletion enhanced tumor regression, and facilitated mild thyroiditis induction. 2) In Her-2 tolerant C57BL/6 mice expressing HLA-DR3, an EAT-susceptibility allele, Her-2 DNA vaccinations must follow Treg depletion for (Her-2xDR3)F1 mice to resist tumor challenge; thyroiditis incidence was moderated by the EAT-resistant IAb allele. 3) In neu tolerant, EAT-resistant BALB/c mice, implanted neu+ tumor also regressed only after Treg depletion and DNA vaccinations. Tumor immunity was long-term, providing protection from spontaneous tumorigenesis. In all three, immune stimuli from concurrent tumor regression and EAT development have a noticeable, mutually augmenting effect. 4) In Treg-depleted, EAT-susceptible CBA/J mice, strong tumor protection was established by immunization with a cell vaccine. mTg injections led to greater thyroiditis incidence and severity. Combination models with MHC class II diversity should facilitate autoimmunity risk assessment and management while generating tumor immunity.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Autoimmunity Reviews - Volume 9, Issue 1, September 2009, Pages 28–33
نویسندگان
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