A study on protective immunity in mice infected with Trichinella spiralis : A new role of IL-3 as Th2 amplifier in immune response to parasite infection

细胞因子平衡是线虫感染产生保护性免疫和病理的关键因素。旋毛虫感染可提高Th2细胞因子和IL-3分泌。我们早期的工作表明(a) IL-3提前了成体螺旋体排出的时间；(b) IL-3增加了肠道肥大细胞和IgE的产生。IL-4已被证明是将B细胞转换为产生IgE所必需的。以上数据表明，IL-3可能在感染过程中通过刺激T细胞和/或B细胞功能影响IgE应答。在目前的研究中，我们已经证明IL-3能够增强IL-4的产生，并且能够分泌IL-4的T细胞被IL-3在体内处理激活和/或诱导。此外，我们还分析了感染螺旋体的淋巴增生突变小鼠的保护性免疫和Th2反应。已经证明，aly/aly小鼠的淋巴增生是由编码NF（核因子）-κB诱导激酶的基因点突变引起的，NF（核因子）-κB诱导激酶是T细胞和B细胞中NF-κB活化的中心介质。在本研究中，我们认为aly基因是诱导螺旋体感染小鼠保护性免疫和Th2应答所必需的。

Cytokine balance is a key factor for the generation of protective immunity and pathology in nematode infections. Infection with Trichinella spiralis elevates Th2 cytokines and IL-3 secretion. Our earlier work showed that (a) IL-3 advanced the timing of adult T.spiralis expulsion ; (b) IL-3 increased both mast cells in the gut and IgE production. IL-4 has been shown to be essential for switching B cells to IgE production. The above data indicate that IL-3 could affect IgE responses by stimulation of T and/or B cell functions during the infection. In the present study we have shown that IL-3 is able to enhance the production of IL-4, and that T cells able to secrete IL-4 are activated and/or induced by in vivo treatment with IL-3. Furthermore, we have analyzed protective immunity and Th2 responses in alymphoplasia mutant mice infected with T.spiralis. It has been demonstrated that alymphoplasia in aly/aly mice is caused by a point mutation in the gene encoding NF (nuclear factor) -κB- inducing kinase which is a central mediator of NF-κB activation in T and B cells. In the present study, we have suggested that aly gene is needed for the induction of protective immunity and Th2 responses in mice infected with T.spiralis.