Cell experiment:

Peripheral blood mononuclear cells are stimulated with PHA (5 mg/mL) along with various concentrations of peptide T (10-6-10-12 M) for 48 h at 37℃. Supernatants are collected and frozen until analysis[3].

Animal experiment:

Rats[4]Peptide T (125, 250, 500, 800 μg) is randomly given subcutaneously to Female Lewis rats aged 6-8 weeks in the hind foot flanks in a final volume of 0.2 mL. Control animals receive the same volume of saline alone[4].

Peptide T is an octapeptide from the V2 region of HIV-1 gp120. Peptide T is a ligand for the CD4 receptor and prevents binding of HIV to the CD4 receptor.

Peptide T acts to block viral entry as it inhibits in the MAGI cell assay and blocks infection in the luciferase reporter assay using HIV virions pseudotyped with ADA envelope. Peptide T selectively inhibits HIV replication using chemokine receptor CCR5 compared to CXC4[2]. Peptide T at 10-8 M induces IL-10 production by the human Th2 cell line and PBMC. Also peptide T at 10-9 M concentration significantly inhibits IFN-g production by PBMC[3].

Peptide T is administered subcutaneously at different doses and phases of the experimental autoimmune encephalomyelitis (EAE) disease, but Peptide T neither prevents nor ameliorates EAE[4].

[1]. Ruff MR, et al. Peptide T[4-8] is core HIV envelope sequence required for CD4 receptor attachment. Lancet. 1987 Sep 26;2(8561):751. [2]. Ruff MR, et al. Peptide T inhibits HIV-1 infection mediated by the chemokine receptor-5 (CCR5). Antiviral Res. 2001 Oct;52(1):63-75. [3]. Raychaudhuri SP, et al. Immunomodulatory effects of peptide T on Th 1/Th 2 cytokines. Int J Immunopharmacol. 1999 Sep;21(9):609-15. [4]. Sáez-Torres I, et al. Peptide T does not ameliorate experimental autoimmune encephalomyelitis (EAE) in Lewis rats. Clin Exp Immunol. 2000 Jul;121(1):151-6.