HIV-1-INDUCED IMMUNE SUPPRESSION MAY RESULT FROM AUTOIMMUNE DISORDERSINCLUDING ANTI-SLWDQ AUTOANTIBODIES

We have previously unravelled the striking SLWDQ pentapeptide identity between HIV-1 env gp120 and the CD4 molecule. We show here that this pentapeptide is required for the functioning of the co-stimulatory MHC -CD4 signal in T4-cell activation since it suppresses antigen-induced T-cell proliferation. Moreover, concerning the MHC class II counterpar t, the LNGQEETGVVSTN sequence which strongly inhibits T-cell immune ac tivation is likely to be part of the functional site of the molecule. Interestingly the MHC/gp120 homology described by Young overlaps this MHC region. We further report that the gp120 SLWDQ peptide triggers an immune reaction which is both humoral (anti-SLWDQ antibodies) and cel lular (CTLs against autologous targets carrying the pentapeptide) in H IV-1 infected individuals. Finally, anti-SLWDQ antibodies from patient s sera purified by column chromatography strongly inhibit antigen-indu ced immune T-cell activation. This result led us to postulate that the se antibodies found in high titers in HIV-1 infected individuals could contribute to set up the progressive systemic immune T-cell suppressi on characterizing AIDS.