A peptide that ameliorates lupus up-regulates the diminished expression of early growth response factors 2 and 3.

Expansion of autoreactive T cells and their resistance to anergy was demonstrated in systemic lupus erythematosus (SLE). A pair of transcription factors, early growth response 2 (Egr-2) and 3 (Egr-3), are negative regulators of T cell activation that were shown to be important in anergy. A peptide (designated hCDR1 for human CDR1) based on the CDR-1 of an anti-DNA Ab ameliorated SLE in both induced and spontaneous lupus models.

Cutting edge: T cells respond to lipopolysaccharide innately via TLR4 signaling.

LPS, a molecule produced by Gram-negative bacteria, is known to activate both innate immune cells such as macrophages and adaptive immune B cells via TLR4 signaling. Although TLR4 is also expressed on T cells, LPS was observed not to affect T cell proliferation or cytokine secretion. We now report, however, that LPS can induce human T cells to adhere to fibronectin via TLR4 signaling.

Chondroitin sulfate-derived disaccharide protects retinal cells from elevated intraocular pressure in aged and immunocompromised rats.

Purpose: A disaccharide (DS) derived from the naturally occurring compound chondroitin sulfate proteoglycan (CSPG) was recently shown to have neuroprotective activity. The authors examined the ability of this compound (CSPG-DS) to protect retinal ganglion cells (RGCs) from death caused by elevated intraocular pressure (IOP).

Methods: With the use of chronic and acute models of elevated IOP, the authors examined the effects of CSPG-DS on RGC survival in adult ( approximately 2 months old), aged (10-12 months old), and immunocompromised Lewis rats.

The negative regulators Foxj1 and Foxo3a are up-regulated by a peptide that inhibits systemic lupus erythematosus-associated T cell responses.

A peptide (hCDR1) based on the complementarity determining region-1 of an anti-DNA antibody ameliorates systemic lupus erythematosus (SLE) in induced and spontaneous lupus models. Our objectives were to determine the effects of hCDR1 on TCR signaling and on its negative regulators, Foxj1 and Foxo3a. BALB/c mice were immunized with the SLE-inducing anti-DNA antibody, designated 16/6Id, and treated with hCDR1.