Therapies that neutralize the function of @entity310 suppress @entity309 ( @entity309 ) but not @entity571 ( @entity571 ). We show that @entity1 suffering from @entity309 but not @entity571 have significant levels of autoantibodies directed to @entity310 . Thus, the immune system can selectively generate @entity792 to proinflammatory mediators when such a response is beneficial for the host. A well-defined model of @entity309 was used to elaborate the contribution of beneficial @entity792 to the regulation of disease. We show that during the disease autoantibody production is elicited against few inflammatory, but not regulatory, mediators. Selective amplification of these beneficial antibodies by targeted DNA vaccines provided protective immunity. Epitope mapping revealed that anti- @entity310 immunity is highly restricted and excretes no crossreactivity to other known gene products. Its selective exclusion substantially exacerbated the disease. Administration of anti- @entity310 antibodies could then override this aggravation. This substantiates the significance of beneficial @entity792 in restraining self-destructive immunity.

Beneficial XXXX to proinflammatory mediators restrains the consequences of self-destructive immunity.

@entity1 :: ('9606', 'Species') :: ['patients'] @entity571 :: ('MESH:D010003', 'Disease') :: ['osteoarthritis', 'OA'] @entity310 :: ('7124', 'Gene') :: ['TNF-alpha'] @entity792 :: ('MESH:D001327', 'Disease') :: ['autoimmunity'] @entity309 :: ('MESH:D001172', 'Disease') :: ['rheumatoid arthritis', 'RA']
@entity792 :: (MESH:D001327,Disease) :: ['autoimmunity']
