Abstract
Abstract M1 protein isolated from group A streptococci, type 1, stimulates human peripheral blood lymphocytes in short-term tissue culture to undergo a dose-dependent increase in DNA synthesis. The degree of this lymphocyte stimulation is not related either to HL-A phenotype, the serum anti-M1 titer of the lymphocyte donor, or the effectiveness of M1 antigen in blocking the cytotoxic activity of HL-A alloantisera. However, both HL-A allo- and heteroantisera are highly effective in specifically inhibiting M1 mitogenic activity. This inhibitory effect clearly depends on anti-HL-A antibody since HL-A alloantisera are rendered ineffective when specifically absorbed with cultured human lymphoid cells. The mechanism by which anti-HL-A antibodies suppress the M1-induced lymphocyte transformation is thought to involve a masking of the M1 protein's mitogenic site such as to prevent interactions with specific lymphocyte receptors required for induction of the proliferative response.
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