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Anti‐ribosomal and ‘P‐peptide’‐specific autoantibodies bind to T lymphocytes

Patients with systemic lupus erythematosus (SLE) frequently have anti‐lymphocyte autoantibodies, some of which also bind to surfaces of neurons. Since anti‐ribosomal P protein autoantibodies (anti‐P) from SLE patients also bind to surfaces of neurons, we hypothesized that anti‐P are anti‐lymphocyte antibodies. A panel of human T lymphocytes was evaluated for anti‐P binding by indirect immunofluorescence. Affinity‐purified anti‐ribosomal antibodies were used as a source of anti‐P. These autoantibodies bound to the surfaces of all transformed T cell lines tested. This binding was not mediated by Fc receptors. It was inhibitable by ribosomes. Anti‐P bound to circulating T lymphocytes from healthy adults and children. They also bound to thymocytes and cord blood T cells from normal neonates. Circulating T cells from SLE patients with anti‐P bound less anti‐P than cells from healthy controls. Two patients were studied on multiple occasions. The capacity of their T cells to bind anti‐P correlated inversely with titres of anti‐ribosomal antibodies. Anti‐ribosomal antibodies, other than anti‐P, also appear to bind to T cells. The surface of T cells contains a protein with the size and antigenicity of the ribosomal P protein, P0. We conclude that anti‐ribosomal antibodies are a subset of anti‐lymphocyte autoantibodies. Their possible role in the pathogenesis of lymphopenia or lymphocyte dysfunction in SLE has to be defined in further studies.