系统性红斑狼疮（systemic lupus erythematosus，SLE）是一种多因素参与的自身免疫性疾病。研究证实，B淋巴细胞、T淋巴细胞、转录因子与细胞因子表达以及抗原呈递等异常或缺陷在SLE的发病中有重要作用，导致包括皮肤、肾、肺、中枢神经系统、消化系统及关节肌肉等多系统、多器官的损伤［1］。SLE患病率约70/10万，目前我国至少有100万以上的患者，尤以育龄期女性多见，其病因及发病机制尚不完全清楚，遗传、环境和病毒感染等因素与其发病关系密切［2］。

Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease, which characterized by complex immunological abnormalities and multiple tissue and organ damages. The etiology and pathogenesis of SLE have not been entirely recognized. Genetic, environmental and viral infections and other factors might be related to the pathogenetic mechanisms of SLE. Interleukin-2 (IL-2) is a critical cytokine produced by T cells upon activation and is important for the generation of T regulatory cells and activation-induced cell death. In SLE patients, T cells display decreased capacity to produce IL-2. Impaired IL-2 expression resulted in decreased generation of regulatory T lymphocytes, and defect of activation-induced cell death. Former researches indicated that IL-2 deficiency in SLE is important for the pathogenesis and treatment of SLE. Several regulating molecules can affect the transcription of IL-2 gene and had an important role in the pathogenesis of SLE. These molecules include cyclic AMP-responsive element modulator (CREM), protein phosphatase 2A (PP2A), E-74 like factor 1 (Elf-1), B lymphocyte induced maturation protein-1 (Blimp-1) and interferon regulator factor 5 (IRF-5). CREM is a transcriptional inhibitor that can repress the transcription of the IL-2 gene by binding to the promoter of the IL-2 gene. PP2A is a Ser/Thr phosphatase that expressed in eukaryotic cells ubiquitously, it represents a negative regulator of the IL-2 gene promoter activity. Elf-1 belongs to the Ets family of transcription factors and can promote the expression of IL-2. Blimp-1 is a crucial transcription factors for regulating B lymphocyte terminal differentiation, an important function of Blimp-1 in T cells is to repress IL-2 gene transcription directly. Interferon regulatory factors (IRFs) are distinctive transcriptional regulators of type Ⅰ interferons (IFNs) and IFN inducible genes, IRF-5 is a member of the IRFs family. IRF-5 is found to be increased in SLE and can regulate the production of IL-2 negatively. PP2A can inhibit the synthesis of IL-2 in two ways: on the one hand, activating the IL-2 transcription inhibitory factor CREMα, on the other hand, inhibiting IL-2 stimulating transcription factor Elf-1. While IRF-5 can activate the IL-2 transcription negative regulator Blimp-1 as to inhibit IL-2 expression. These molecules participate in the regulation of IL-2 through different pathways. This paper reviews the current knowledge of IL-2 signaling pathway regulating molecules in SLE.