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Decreased level of thymidine in the serum of obese strain (OS) chickens with spontaneous autoimmune thyroiditis.

We have previously shown that normal chicken serum (NCS) is able to interfere with the IL 2 promoted incorporation of DNA precursors into T lymphoblasts and that serum derived from autoimmunity prone Obese strain (OS) chickens is deficient in this respect. This "defect in non-specific suppression" has been speculated to be one of the causes for T cell hyperreactivity in the OS. In this study we present several lines of evidence that the suppressive effect of normal chicken serum (NCS) on 5-(125Iodo)-2-deoxyuridine (125IUdR) uptake into chicken T blasts is a competition artefact due to cold thymidine (TdR) present in NCS. Inhibition of 125IUdR required the continuous presence of NCS and suppression of 3H-TdR incorporation could be competed for by increasing the dose of the radiolabel. Molecular sieve chromatography followed by reversed phase high performance liquid chromotagraphy revealed the "inhibitory" activity to co-elute with TdR. Moreover, NCS did not suppress protein synthesis by chicken T cells growing with IL 2 and did not affect oxidative metabolism, cell viability, expression of IL 2 receptors, or percentages of cells in the S phase of the cell cycle. In accordance with these data, OS-sera suprisingly contain less TdR than those from normal controls. Experiments involving crosses of the OS with the normal inbred CB strain, revealed that the subnormal serum TdR level of the OS is an autosomally dominant trait which, however, segregates from T cell hyperreactivity. These findings falsify our previous hypothesis that a defect in specific IL 2 antagonists might be involved in T cell hyperfunction of the OS and indicate that NCS is devoid of factors which neutralize IL 2 function.