Basophils and the T helper 2 environment can promote the development of lupus nephritis.
Basophils and the T helper 2 environment can promote the development of lupus nephritis.
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在系统性红斑狼疮（SLE）中，自身反应性抗体可靶向肾脏（狼疮性肾炎），导致肾功能衰竭甚至可能死亡。我们报道，自身反应性IgE激活嗜碱性粒细胞，使其归巢到淋巴结，促进TH2细胞分化，并增强自身反应性抗体的产生，从而在Lyn - / - 小鼠中引发狼疮样肾炎。SLE患者的血清IgE、自身反应性IgE以及表达CD62L和MHC II类分子HLA - DR的活化嗜碱性粒细胞也升高；这些参数被发现与疾病活动增加和活动性狼疮性肾炎有关。嗜碱性粒细胞也存在于SLE患者的淋巴结和脾脏中。因此，在Lyn - / - 小鼠中，嗜碱性粒细胞和IgE自身抗体放大了导致狼疮性肾炎的自身抗体产生，并且在SLE患者中，IgE自身抗体和活化嗜碱性粒细胞的存在是与疾病活动和肾炎相关的因素。
In systemic lupus erythematosus (SLE) self-reactive antibodies can target the kidney (lupus nephritis) leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE, causes their homing to lymph nodes, promoting TH2 cell differentiation, and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in Lyn−/− mice. SLE patients also have elevated serum IgE, self-reactive IgE's, and activated basophils that express CD62L and the MHC Class II molecule, HLA-DR; parameters that were found to be associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of SLE patients. Thus, in Lyn−/− mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in SLE patients, the presence of IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.