The aim of this work was to study the expression of human leukocyte antigen G (HLA-G) and interleukin 10 (IL-10) in conjunction with expression of HLA-G killer-cell inhibitory receptor ligand immunoglobulin-like transcript 2 (ILT2) in CD3+, CD19+, CD56+ lymphomas, and ILT4 in CD14+ cells from patients with systemic lupus erythematosus (SLE). Thirty-one SLE patients and 36 healthy controls were studied. ILTs expression was analyzed by flow cytometry in peripheral blood mononuclear cells (PBMCs). The plasma sHLA-G and IL10 were evaluated by enzyme-linked immunosorbent assay (ELISA). We found a significant increased expression of ILT2 by lymphocytes in SLE patients. When the expression of this receptor was assessed in cell subsets, significantly higher ILT2 MRFI levels were detected in CD3+ cells, CD19+ cells, CD56+ cells (P < 0.05), but no change with ILT4 MRFI in CD14+ cells, neither did the percentages of ILT2/4+ lymphocytes change in SLE patients compared with healthy controls (P > 0.05). The upregulation of ILT2 expression was related to IL10 and anti-ds-DNA antibodies (P < 0.05), but not sHLA-G and steroid therapy (P > 0.05). IL-10 and sHLA-G were increased, but did not change remarkably (P > 0.05); however, they were quite related (P < 0.05). ILT2 might be one of the factors accounting for the evasion of immunosurveillance, thus participate in the pathogenesis of SLE, and the upregulation of ILT2 may be associated with its disease activity.