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Stimulation of Lymphocyte Transformation by Streptococcal Type M1 Protein: Relationship to HL-A Antigens¹

From the Scripps Clinic and Research Foundation, La Jolla, California 92037, the Abbott Laboratories, North Chicago, Illinois 60064, and the University of California School of Medicine, Los Angeles, California 90024

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.

Footnotes

¹ This is Publication No. 570 from the Department of Experimental Pathology, Scripps Clinic and Research Foundation, La Jolla, California 92037. This work was supported by United States Public Health Service Grants AI 10180 and CA 10596 from the National Institutes of Health and Grant 70-615 from the American Heart Association, Inc.

² Scripps Clinic and Research Foundation, La Jolla, California 92037.

³ Abbott Laboratories, North Chicago, Illinois 60064.

⁴ University of California School of Medicine, Los Angeles, California 90024.