Experimental evidence presented in this paper suggests that the T cell hyperreactivity of NZB mice against H-2 identical target cells is a true primary response and not the consequence of an in vivo T cell autoimmune priming event. Based on additional data, we believe an elevated potential of T cell help to be present in NZB mice, which facilitates the observed hyperreactivity F1 hybrids of NZB and normal strains of mice inherited the capacity to hyperreact against H-2 identical cells in an H-2-unrestricted fashion. Because the hybrids tested possess both Qa-1 alleles--Qa-1b and Qa-1a--our experiments either indicate the existence of heterogeneity within the Qa-1b system or of an H-2-unrestricted response against additional target antigens. The T cell hyperreactivity might prove to be a valuable tool in further investigations of the pathomechanism of autoimmune disease.