PubMed1975
Allotype suppression is held to be an example of T-cell suppressor function. Failure of generalized suppressor T-cell function is considered to be responsible for the chronic and progressive disease of the NZB. The possible association of allotype suppression and autoimmune disease has been investigated here in a group of NZB mice, transplanted and born from BALB/c recipients whilst producing anti-NZB allotype. In this situation it was anticipated that if allotype suppression should fail this would coincide with the development of autoimmune disease; both processes reflecting failure of T-cell suppressor function. However, in spite of the fact that allotype suppression was not achieved, certain observations seem important. The fact that NZB born the BALB/c were in no way different from normally derived NZB confirms that the cause of the NZB disease is established prior to the stage of implantation. Maternal influence at or beyond this stage appears of little consequence in terms of effecting the development or progression of the NZB disease. The failure to induce allotype suppression in the NZB is important. In this context this strain appears to be no different from the majority of other strains that have been tested as homozygotes. The suppression obtained with (BALB/c X SJL/J)F1 hybrids in which chronic suppression has been achieved therefore seems to represent an exceptional situation and this suggests that it is perhaps unwise to base general assumptions as to the universal adaptability of T-cell control mechanisms upon unusual findings. It must be remembered that only homozygotes were examined here. Earlier attempts to induce allotype suppression in homozygotes also failed, even in the SJL/J. Since allotype suppression has only been demonstrated in heterozygote mice there is a distinct possibility that this phenomenon never occurs in the homozygote situation. The significance of this possibility is discussed.