1. ¹Laboratory of Immunology, Brest University Medical School, Brest, France
2. ²Laboratory of Virology, Brest University Medical School, Brest, France

Correspondence: Professor P Youinou, Laboratory of Immunology, Brest University Medical School Hospital, 2 avenue Foch, BP824, F 29609 Brest, France. E-mail: youinou@univ-brest.fr

Received 26 April 2005; Revised 6 July 2005; Accepted 6 July 2005; Published online 18 August 2005.

Abstract

All T lymphocytes and some B lymphocytes express CD5. This coreceptor is encoded by one gene that consists of 11 exons. We have previously described a B cell-specific alternative exon 1, leading to the synthesis of a protein, devoid of leader peptide, and, therefore, retained in the cytoplasm. The novel exon 1 originates from a human endogenous retrovirus (HERV) at a time interval between the divergence of New World monkeys from Old World monkeys, and prior to the divergence of humans from Old World monkeys. Based on sequence similarity to -retroviruses, it was categorized as class I: based on the specificity of its primer binding site, it was allotted to the subclass E, and based on its location within the cd5 gene, named HERV-E.CD5. Alternative transcripts were detected in lymphoid organs including fetal liver (not adult liver), more particularly in CD5-negative cell surface B-1b than in CD5-positive cell surface B-1a, and not at all in B-2 cells. By alignment of 5' long terminal repeats, HERV-E.CD5 was distinguished from similar proviruses. This could be central to the regulation of membrane expression of CD5 in human B lymphocytes, and, thereby, to the strength of the B-cell antigen receptor signaling.