[Lymphocyte activation by bacterial biostructures: precursor of infection-induced immune phenomena and sequelae? I. lymphocyte reactions to A-streptococci].

The pathogenesis of the nonsuppurative sequelae of bacterial infections, e.g. rheumatic fever (RF) following A-streptococcal infection and seronegative spondarthritis (SS) following enterobacterial infection, is thought to be related to 1. an unusual persistence of infection, and/or 2. direct toxic effects of bacterial toxins, and/or 3. an abnormal immune response to the inital infection. Additionally, modern working hypothesis center around more recent findings concerning the genetic predisposition (for which there are now markers in both diseases) and the various immunologically active biostructures of the bacteria. These structures consist chiefly of a. crossreactive (CR) antigens, i.e. common or similar epitopes in both bacteriae and mammalian tissues, and b. polyclonal cell activators, e.g. the polyclonal B-cell activator (PBA) which induce immunologically many nonspecific resting B-cell clones to mature into Ig secreting cells. In this paper the lymphocyte response to a wide range of bacterial cell preparations is described. Blood lymphocytes from both RF and SS patients respond to the disease-precipitating microorganism more rigorously than the controls. There are several lines of evidence that the heightened response is genetically determined. However, there are no obvious facts which can confirm the idea that the so-called cross-reactive antigen preparations induce a specific cell response to CR antigens. On the contrary, such crude cell membrane preparations are obviously composed of an antigenic mosaic and of polyclonal cell activators: lymphocytes from healthy blood donors and even from newborns respond with lymphokine production, blastogenesis and Ig secretion under certain circumstances.(ABSTRACT TRUNCATED AT 250 WORDS)