In vitro T cell hyperreactivity in Obese strain (OS) chickens is due to a defect in nonspecific suppressor mechanism(s).
Spontaneous autoimmune thyroiditis of OS chickens is associated with a marked hyperreactivity of the T cell system. The purpose of the present study was to investigate the underlying regulatory mechanisms. Co-cultivation experiments between Con A-stimulated OS and NWL lymphocytes in communicating cultures revealed soluble regulatory factors to be responsible for the observed functional differences: the high proliferative response to Con A and hyperproduction of IL 2 of OS cells was found to be due to a deficiency in the conditioned medium of dialyzable inhibitory factor(s) that regulate IL 2 secretion of NWL lymphocytes. Furthermore, sera of young NWL chickens were found to profoundly inhibit the IL 2-promoted lymphoblast proliferation. This IL 2 antagonizing activity is lost with age (3 to 6 yr) and was found to be significantly diminished in OS birds throughout ontogeny, thus pointing to possible parallels between immune regulatory dysfunction in autoimmunity and in physiologic aging. Both enhanced T cell response and the defect in serum suppressor were inherited by (OS X CB)F1 animals, indicating that these two aberrations may be related to each other.
D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology; D002645:Chickens / Q000276:immunology*; D003470:Culture Media; D006023:Glycoproteins / Q000235:genetics / Q000502:physiology; D007153:Immunologic Deficiency Syndromes / Q000235:genetics / Q000276:immunology*; D007376:Interleukin-2 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000235:genetics / Q000502:physiology*; D009363:Neoplasm Proteins; D013491:Suppressor Factors, Immunologic; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
D003470:Culture Media; D006023:Glycoproteins; D007376:Interleukin-2; D008222:Lymphokines; D009363:Neoplasm Proteins; D013491:Suppressor Factors, Immunologic; C038588:serum immunosuppressive factor, human