Splenocytes from the motheaten mouse, after stimulation with alloantigen, lack the ability to utilize exogenous interleukin 1 (IL 1) or interleukin 2 (IL 2), express receptors for IL 2, or produce (IL 2). However, in contrast to other models of autoimmunity and immunodeficiency, after mitogen stimulation, motheaten splenocytes produced as much IL 1 or IL 2 as their normal littermates. In addition, these splenocytes expressed functional IL 2 receptors in the same quantity as normal littermate or wild-type splenocytes. Furthermore, motheaten thymocytes and splenocytes, like their normal littermates, respond synergistically to IL 1 on co-stimulation with mitogen, suggesting expression of an IL 1 receptor. Thus, motheaten mouse splenocytes are unable to utilize an antigen-delivered signal and convert it into cytokine production or IL 2 receptor expression. If the antigen signal is bypassed with mitogen, cytokine production and receptor expression appear normal.

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