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THE DISEASE OF THE NZB MOUSE II. FURTHER STUDIES ON TETRAPARENTAL NZB ? CFW CHIMAERAS DERIVED BY AGGREGATION OF EARLY EMBRYOS
Author(s) -
Barnes R. D.,
Wills E. J.,
Tuffrey Maureen
Publication year - 1975
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1975.tb00523.x
Subject(s) - biology , autoantibody , immunology , disease , phagocytosis , chimera (genetics) , autoimmune disease , autoimmunity , receptor , embryo , clonal deletion , antibody , genetics , t cell , t cell receptor , immune system , medicine , pathology , gene
SUMMARY Further evidence supporting the hypothesis that the autoimmune disease of the NZB results from failure of T cell mediated autoimmune suppressor function has been obtained from ovum fusion‐derived tetraparental NZB ? CFW chimaeras. Although the issue was complicated in three chimaeras by an acute interaction between the two parental strain cell populations, one animal remained well and no evidence of disease was found at postmortem. Electron microscopy demonstrated large numbers of C‐type particles in all the chimaeras and renal changes of an acute type rather than chronic NZB disease in two of the animals. Erythrophagocytosis was observed in all the chimaeras and was probably initiated by an antiautoantibody receptor‐determinant reaction. The phagocytosis of plasma cells suggested that the reaction was also directed against the clonal source of the autoantibody. A similar receptor‐determinant reaction may be responsible for the ‘normal’ elimination of aberrant autoimmune clones.