摘要：

Niels Jerne published a theory on the network regulation of immune responses, which briefly states that antigen introduced into the organism induces the formation of specific antibodies and, in turn, the production of specific anti-idiotypic antibodies. Anti-idiotypic antibodies therefore compete with antigen for the binding site of the primary antibodies. Since antigenic determinants therefore might cross-react with idiotypic determinants, the repertoire of the immune system would be as efficient if it were primarily directed against the idiotypic determinants themselves. The efficiency of recognition would be equal in both instances. This implies that immunoglobulins could be the primary recognition targets for the B-lymphoid cells. There is no direct relationship between Jerne's idea and the argument that the anti-Ig antibodies that occur in RA patients and react primarily with constant parts of Ig molecules reflect a similar kind of network. However, this argument has found experimental support in studies by Dresser. Injection of a PBA into mice, which induces polyclonal antibody formation, leads to an unproportionally large fraction of activated B cells that produce antibodies against immunoglobulin and corresponds to RF activity. Dresser also showed that polyclonal anti-Ig antibodies constitute a significant part of all specific immune responses. Furthermore, Coutinho et al. have found that certain anti-idiotypic antibodies can act as physiological PBA substances and might therefore serve the function of true growth-promoting factors and driving force for the continous proliferation of the B-lymphoid system. This interesting finding will probably have a great impact on basic immunological theory in the near future. Finally, investigations by Natvig's group have further indicated that a large proportion of B lymphocytes of RA patients have the capacity to secrete RF idiotype-bearing immunoglobulins. Probably as many as 10% of all peripheral B lymphocytes can be engaged in antibody synthesis with RF activity. In the light of these findings it may be fruitful to study the role of non-specific activation of immune responses in various diseases characterized by the formation of a heterogeneous group of autoantibodies. Examples of such diseases are, in addition to RA, juvenile RA and SLE.

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