Shenker B J, Willoughby W F, Hollingdale M R, Mann T N
J Immunol. 1980 Apr;124(4):1763-72.
We have previously shown that inhaled Con A has a powerful enhancing effect on the formation of immune complexes between an inhaled antigen and circulating antibody. Immunohistochemical staining has demonstrated such complexes, together with host complement, in close association with foci of necrotizing destruction of the pulmonary parenchyma. We have postulated that Con A promotes immune complex formation indirectly through polyclonal activation of lymphocytes in the lung. In this paper we test this hypothesis in animals rendered unresponsive to Con A stimulation in vivo by i.v. administration of cholera toxin (CT). Such treatment raised the levels of cAMP in peripheral blood lymphocytes and inhibited their proliferative response to Con A in vitro. CT administration further blocked the local inflammatory response to intradermal injections of Con A, as well as the cell-mediated immune response to intradermal injections of BSA. Although CT failed to block the immune complex-mediated Arthus vasculitis in the skin, it did block production of immune complex pulmonary injury by antigen/mitogen aerosols, as did decomplementation with purified cobra venom factor. These findings support the hypothesis that polyclonal activation of pulmonary lymphocytes promotes immune complex-type alveolitis, possibly by facilitating interactions between humoral antibody and intra-alveolar antigen.
我们之前已经表明，吸入的伴刀豆球蛋白A（Con A）对吸入抗原与循环抗体之间免疫复合物的形成具有强大的增强作用。免疫组织化学染色已证实此类复合物以及宿主补体与肺实质坏死性破坏灶紧密相关。我们推测Con A通过肺中淋巴细胞的多克隆激活间接促进免疫复合物的形成。在本文中，我们通过静脉注射霍乱毒素（CT）使动物在体内对Con A刺激无反应，从而验证这一假设。这种处理提高了外周血淋巴细胞中的环磷酸腺苷（cAMP）水平，并抑制了它们在体外对Con A的增殖反应。CT给药进一步阻断了对皮内注射Con A的局部炎症反应，以及对皮内注射牛血清白蛋白（BSA）的细胞介导免疫反应。尽管CT未能阻断皮肤中免疫复合物介导的阿瑟斯血管炎，但它确实像用纯化的眼镜蛇毒因子进行补体灭活一样，阻断了抗原/丝裂原气雾剂引起的免疫复合物性肺损伤。这些发现支持了以下假设，即肺淋巴细胞的多克隆激活可能通过促进体液抗体与肺泡内抗原之间的相互作用来促进免疫复合物型肺泡炎。
