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Rats were immunized by one to eight intraperitoneal administrations of species-homologous kidney fractions (prepared according to Ryan's differential centrifugation technique) emulsified in Freund's complete adjuvant. Proliferative and membranous glomerulitis ensued in about one-third of animals receiving five or more injections of any of the four renal preparations, i.e. heavy particle, mitochondrial, microsomal and soluble fractions. A significant increase in the in- cidence and titre of complement-fixing antibodies to renal antigens occurred, beginning with the third injection in rats sensitized with the heavy particle material and soluble fraction, and possibly also with the microsomal fraction; the mitochondrial fraction was ineffective in this respect. In this as in previous studies, neither a positive nor a negative correlation was established between the development of renal disease and the formation of circulating antibodies, glomerulitis frequently being found in the absence of detectable antibodies and vice versa. It is hypothesized that immunization with renal antigens elicits an immune response in the wake of which two independent processes are observed, namely the development of renal disease and the formation of circulating antibodies. [ABSTRACT FROM AUTHOR]

Acute sialoadenitis, ascribed to local formation of immune complexes, develops in sensitized rats after a single intraductal challenge with the sensitizing antigen. Multiple intraductal challenges induce a state of non-reactivity of the organ characterized by a lack of inflammatory reaction to the sensitizing antigen. This non-reactivity is antigen-specific, since introduction of ovalbumin, after multiple intraductal instillations of bovine serum albumin (BSA), elicits an inflammatory response in animals immunized with the two antigens. At the same time, instillation of BSA into the contralateral gland, which has not been challenged, causes acute adenitis. Anti-BSA antibodies are detected in the serum and parotid saliva at the time of refractoriness of the gland. The phenomenon is a transient one since the faculty of the salivary gland to respond by an inflammatory reaction recovers after a challenge-free period. These experiments bring to light a new phenomenon, the possible mechanisms of which are discussed. [ABSTRACT FROM AUTHOR]

The parotid gland and knee joint of immunized ruts were challenged with the sensitizing antigen. Sialoadenitis developed in over half of these rats alter one and three challenges via the parotid duct. On the other hand, most glands were normal after five, seven and eight intraductal challenges in spite of the presence of precipitating antibodies in the serum and hemagglutinating antibodies in the parotid saliva; in only a few animals did chronic destructive adenitis ensue. This contrasted with the incidence and severity of synovitis, which increased with the number of intra-articular injections of antigen, The non-reactivity of the gland is antigen specific in as much as acute adenitis resulted from intraductal instillation of a second antigen following multiple challenges with another one in rats sensitized with two antigens. The results evince a difference in the local reactivity between the salivary gland and synovial membrane. [ABSTRACT FROM AUTHOR]