Immunity to infection has been extensively studied in humans and mice bearing naturally occurring or experimentally introduced germline mutations. Mouse studies are sometimes neglected by human immunologists, on the basis that mice are not humans and the infections studied are experimental and not natural. Conversely, human studies are sometimes neglected by mouse immunologists, on the basis of the uncontrolled conditions of study and small numbers of patients. However, both sides would agree that the infectious phenotypes of patients with inborn errors of immunity often differ from those of the corresponding mutant mice. Why is that? We argue that this important question is best addressed by revisiting and reinterpreting the findings of both mouse and human studies from a genetic perspective. Greater caution is required for reverse-genetics studies than for forward-genetics studies, but genetic analysis is sufficiently strong to define the studies likely to stand the test of time. Genetically robust mouse and human studies can provide invaluable complementary insights into the mechanisms of immunity to infection common and specific to these two species.

中文翻译：

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在遗传学坛上协调小鼠和人类免疫学

感染免疫已在携带自然发生或实验引入种系突变的人类和小鼠中进行了广泛研究。人类免疫学家有时会忽视小鼠研究，因为小鼠不是人类，而且研究的感染是实验性的而非自然的。相反，由于研究条件不受控制和患者数量较少，人类研究有时会被小鼠免疫学家忽视。然而，双方都同意，先天性免疫缺陷患者的感染表型通常与相应突变小鼠的感染表型不同。这是为什么？我们认为，最好通过从遗传学角度重新审视和解释小鼠和人类研究的结果来解决这个重要问题。与正向遗传学研究相比，反向遗传学研究需要更加谨慎，但遗传分析足够强大，可以定义可能经得起时间考验的研究。遗传稳健的小鼠和人类研究可以为这两个物种常见和特异的感染免疫机制提供宝贵的补充见解。