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The article presents a study on the use of the peptide human first complementarity-determining region (hCDR1) in ameliorating the central nervous system (CNS) pathology in mice with systemic lupus erythematosus (SLE). It is stated in the study that hCDR1 reduced pathologic cytokine production. It notes that the study determined the cytokine expression and assessed anxiety-like behavior. It also mentions that the study found that CNS pathology was reduced by hCDR1 treatment.

Abstract: Interferon-γ (IFN-γ) plays a pathogenic role in systemic lupus erythematosus (SLE). Uncontrolled IFN-γ signaling may result from a deficiency in the negative regulator, namely, suppressor of cytokine signaling-1 (SOCS-1). We investigated the activation status of IFN-γ signaling pathway in SLE-afflicted (New-Zealand-Black×New-Zealand-White)F1 mice and determined its responsiveness when treating with a tolerogenic peptide, hCDR1, which ameliorates SLE. SOCS-1 was suppressed and pSTAT1 was enhanced in spleen-derived cells from SLE-affected mice as compared with healthy controls. Treatment with hCDR1 reversed the expression of these two molecules in association with clinical amelioration. In vitro stimulation with IFN-γ resulted in elevated levels of SOCS-1 in cells from both vehicle and hCDR1-treated mice but this effect reached significance only in cells of the latter group, which also exhibited reduced levels of pSTAT1. Thus, SOCS-1 is diminished in SLE-affected mice, and treatment with hCDR1 results in its up-regulation thereby restoring control of IFN-γ signaling pathway. [Copyright &y& Elsevier]