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首页> 外文期刊>Infection and immunity >Oral immunization of interleukin-4 (IL-4) knockout mice with a recombinant Salmonella strain or cholera toxin reveals that CD4+ Th2 cells producing IL-6 and IL-10 are associated with mucosal immunoglobulin A responses.
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Oral immunization of interleukin-4 (IL-4) knockout mice with a recombinant Salmonella strain or cholera toxin reveals that CD4+ Th2 cells producing IL-6 and IL-10 are associated with mucosal immunoglobulin A responses.

机译：用重组沙门氏菌菌株或霍乱毒素对白介素4（IL-4）敲除小鼠进行口服免疫后发现，产生IL-6和IL-10的CD4 + Th2细胞与粘膜免疫球蛋白A反应有关。

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Mucosal immunoglobulin A (IgA) responses are often associated with Th2-type cells and derived cytokines, and interleukin-4 (IL-4) knockout (IL-4-/-) mice with impaired Th2 cells respond poorly to oral antigens. However, we have noted that IL-4-/- mice have normal mucosal IgA levels, which led us to query whether different oral delivery systems could elicit mucosal immunity. Two oral regimens were used: (i) a live recombinant Salmonella strain which expresses fragment C (ToxC) of tetanus toxin, and (ii) soluble tetanus toxoid (TT) with cholera toxin (CT) as an adjuvant. Oral immunization of IL-4-/- mice with recombinant Salmonella vaccine expressing ToxC induced brisk mucosal IgA and serum IgG (mainly IgG2a) anti-TT antibody responses. TT-specific CD4+ T cells from spleen or Peyer's patches produced gamma interferon, indicative of Th1 responses; however, IL-6 and IL-10 were also seen. Oral immunization of IL-4-/- mice with TT and CT induced weak mucosal IgA to TT; however, brisk IgA anti-CT-B responses and CT-B-specific CD4+ T cells producing IL-6 and IL-10 were also noted. These results show that although IL-4-dependent antibody responses are impaired, mucosal IgA responses are induced in IL-4-/- mice. These result suggest that certain cytokines, i.e., IL-6 and IL-10 from Th2-type cells, play an important compensatory role in the induction and regulation of mucosal IgA responses.
机译：粘膜免疫球蛋白A（IgA）反应通常与Th2型细胞和衍生的细胞因子有关，Th2细胞受损的白细胞介素4（IL-4）敲除（IL-4-/-）小鼠对口服抗原的反应较差。但是，我们注意到IL-4-/-小鼠的粘膜IgA水平正常，这使我们质疑不同的口服给药系统是否可以引起粘膜免疫。使用两种口服方案：（i）表达破伤风毒素片段C（ToxC）的活重组沙门氏菌菌株，和（ii）以霍乱毒素（CT）为佐剂的可溶性破伤风类毒素（TT）。用表达ToxC的重组沙门氏菌疫苗对IL-4-/-小鼠进行口服免疫，诱导轻度粘膜IgA和血清IgG（主要是IgG2a）抗TT抗体反应。来自脾脏或Peyer斑块的TT特异性CD4 + T细胞产生γ干扰素，表明Th1反应。然而，也观察到IL-6和IL-10。用TT和CT对IL-4-/-小鼠进行口服免疫可诱导TT产生弱的粘膜IgA。然而，也注意到活跃的IgA抗CT-B反应和产生IL-6和IL-10的CT-B特异性CD4 + T细胞。这些结果表明，尽管IL-4依赖性抗体应答受损，但是在IL-4-/-小鼠中诱导了粘膜IgA应答。这些结果表明，某些细胞因子，即来自Th2型细胞的IL-6和IL-10，在粘膜IgA应答的诱导和调节中起重要的补偿作用。

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