| Summary: | <p>Mutation in the “nude” gene, i.e. the <i>FoxN1</i> gene, induces a hairless phenotype and a rudimentary thymus gland in mice (nude mouse) and humans (T-cell related primary immunodeficiency). Conventional <i>FoxN1</i> gene knockout and transgenic mouse models have been generated for studies of <i>FoxN1</i> gene function related to skin and immune diseases, and for cancer models. It appeared that FoxN1's role was fully understood and the nude mouse model was fully utilized. However, in recent years, with the development of inducible gene knockout/knockin mouse models with the <i>loxP</i>-Cre(ER<sup>T</sup>) and diphtheria toxin receptor-induced cell abolished systems, it appears that the complete repertoire of FoxN1's roles and deep-going usage of nude mouse model in immune function studies have just begun. Here we summarize the research progress made by several recent works studying the role of <i>FoxN1</i> in the thymus and utilizing nude and “second (conditional) nude” mouse models for studies of T-cell development and function. We also raise questions and propose further consideration of <i>FoxN1</i> functions and utilizing this mouse model for immune function studies.</p>
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