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首页> 外文期刊>Allergy >CD25+ regulatory T cells transfer n-3 long chain polyunsaturated fatty acids-induced tolerance in mice allergic to cow's milk protein
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CD25+ regulatory T cells transfer n-3 long chain polyunsaturated fatty acids-induced tolerance in mice allergic to cow's milk protein

机译：CD25 +调节性T细胞转移n-3长链多不饱和脂肪酸诱导的对牛奶蛋白过敏的小鼠的耐受性

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Background Recently, we have shown that dietary long-chain n-3 polyunsaturated fatty acids (n-3 LCPUFA) largely prevent allergic sensitization in a murine model for cow's milk allergy. The aim of this study was to assess the contribution of regulatory T cells (Treg) in the prevention of food allergy by n-3 LCPUFA. Methods C3H/HeOuJ female donor mice were fed a control or fish oil diet before and during oral sensitization with cow's milk protein whey. Acute allergic skin response (ASR), anaphylaxis, body temperature, serum immunoglobulins, and mouse mast cell protease-1 (mmcp-1) were assessed. Splenocytes of sham- or whey-sensitized donor mice fed either control or fish oil diet were adoptively transferred to na?ve recipient mice. Recipient mice received a whole splenocyte suspension, splenocytes ex vivo depleted of CD25+ cells, or MACS-isolated CD4+ CD25+ Treg. Recipient mice were sham- or whey-sensitized and fed control diet. Results The ASR as well as whey-specific IgE and whey-specific IgG1 levels were reduced in whey-sensitized donor mice fed the fish oil diet as compared to the control diet. Splenocytes of control-diet-fed whey-sensitized donors transferred immunologic memory. By contrast, splenocytes of fish-oil-fed whey-sensitized - but not sham-sensitized - donors transferred tolerance to recipients as shown by a reduction in ASR and serum mmcp-1, and depletion of CD25+ Treg abrogated this. Transfer of CD25+ Treg confirmed the involvement of Treg in the suppression of allergic sensitization. Conclusions CD25+ Treg are crucial in whey allergy prevention by n-3 LCPUFA.
机译：背景技术最近，我们已经表明，在鼠类对牛奶过敏的模型中，饮食中的长链n-3多不饱和脂肪酸（n-3 LCPUFA）在很大程度上防止了过敏性致敏。这项研究的目的是评估n-3 LCPUFA对调节性T细胞（Treg）在预防食物过敏中的作用。方法在对C3H / HeOuJ雌性供体小鼠进行口服敏化之前和期间，用牛奶蛋白乳清喂养对照或鱼油饮食。评估了急性过敏性皮肤反应（ASR），过敏反应，体温，血清免疫球蛋白和小鼠肥大细胞蛋白酶1（mmcp-1）。饲喂对照或鱼油饮食的假或乳清致敏供体小鼠的脾细胞被过继转移至幼稚的受体小鼠。受体小鼠接受了完整的脾细胞悬液，离体的脾细胞耗尽了CD25 +细胞或MACS分离的CD4 + CD25 + Treg。接受伪造或乳清致敏的小鼠，喂饲对照饮食。结果与喂食鱼油饮食相比，喂食鱼油饮食的乳清致敏供体小鼠的ASR以及乳清特异性IgE和乳清特异性IgG1水平均降低。对照饮食喂养的乳清敏化供体的脾细胞转移了免疫记忆。相比之下，鱼油喂养的乳清致敏而不是假刺激致敏的脾细胞将耐受性转移给了受体，如ASR和血清mmcp-1的减少所表明的，CD25 + Treg的消耗消除了这种情况。 CD25 + Treg的转移证实了Treg参与了过敏性致敏的抑制。结论CD25 + Treg在n-3 LCPUFA预防乳清过敏中至关重要。

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