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DQ 65–79, a Peptide Derived from HLA Class II, Induces IB Expression¹

Yun Jiang^*, Daniel Chen, Shu-Chen Lyu^*, Xuefeng Ling, Alan M. Krensky and Carol Clayberger^2,*,

^* Department of Cardiothoracic Surgery and Division of Immunology and Transplantation Biology, Department of Pediatrics, Stanford University, Stanford, CA 94305

A synthetic peptide corresponding to residues 65–79 of the helix of the -chain of the class II HLA molecule DQA03011 (DQ 65–79) inhibits the proliferation of human T lymphocytes in an allele nonrestricted manner. By using microarray technology, we found that expression of 29 genes was increased or decreased in a human CTL cell line after treatment with DQ 65–79. This study focuses on one of these genes, IB-, whose expression is increased by DQ 65–79. IB proteins, including IB- and IB-, are increased in T cells treated with DQ 65–79. Nuclear translocation of the NF-B subunits p65 and p50 is decreased in T cells after treatment with DQ 65–79, while elevated levels of p65 and p50 are present in cytosol. DQ 65–79 inhibits the degradation of IB- mRNA and inhibits the activity of IB kinase. These findings indicate that the DQ 65–79 peptide increases the level of IB proteins, thereby preventing nuclear translocation of the transcription factor, NF-B, and inhibiting T cell proliferation.

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