Sarcocystis neurona is the predominant etiological agent of the infectious equine neurologic disease, equine protozoal myeloencephalitis (EPM), which is prevalent in the United States. A wealth of knowledge about S. neurona biology and its life cycle has accumulated over the last several decades. However, much remains unknown about the aberrant equine host’s immune response to S. neurona and the relatively high prevalence of exposure to the protozoa but relatively infrequent occurrence of clinical neurologic disease. Mouse models simulating EPM are commonly used to study the disease due to numerous challenges associated with studying the disease in horses. The critical role of the cytokine, interferon gamma (IFNγ), in protection against S. neurona encephalitis has been well established as Ifnγ^−/− mice are highly susceptible to S. neurona encephalitis. However, there are discrepancies in the literature regarding S. neurona disease susceptibility in lymphocyte deficient mice, lacking T-lymphocytes and their associated Ifnγ production. In the current study, we investigated S. neurona encephalitis susceptibility in 2 genetically different strains of lymphocyte null mice, C57Bl/6 (B6).scid and Balb/c.scid. The B6.scid mouse was determined to be susceptible to S. neurona encephalitis as 100 % of infected mice developed neurologic disease within 60 days post infection (DPI). The Balb/c.scid mouse was nearly disease resistant as only 10 % of mice developed neurologic disease 60 DPI. Encephalitis was histologically demonstrable and S. neurona was identified in cerebellar samples collected from B6.scid but absent in Balb/c.scid mice. To further investigate the importance of T-lymphocyte derived Ifnγ, T- lymphocytes were adoptively transferred into B6.scid mice. The adoptive transfer of Ifnγ competent T- lymphocytes offered complete protection against S. neurona encephalitis but transfer of Ifnγ deficient T- lymphocytes did not with 100 % of these recipient mice succumbing to S. neruona encephalitis. Histological analysis of collected cerebellar samples confirmed the presences of S. neurona and encephalitis in recipient mice that developed neurologic disease. These studies show that the background strain is critical in studying SCID susceptibility to S. neurona disease and suggest a protective role of Ifnγ producing T- lymphocytes in S. neurona encephalitis susceptible mice.

肉孢子虫神经元是传染性马神经系统疾病马原生动物脊髓脑炎 (EPM) 的主要病原体，该疾病在美国很普遍。在过去的几十年里，积累了大量关于S. 神经元生物学及其生命周期的知识。然而，关于异常马宿主对S.neurona的免疫反应以及接触原生动物的相对较高的流行率但临床神经系统疾病的发生率相对较低，仍有很多未知之处。由于与研究马疾病相关的众多挑战，模拟 EPM 的小鼠模型通常用于研究该疾病。细胞因子、干扰素 γ (IFNγ) 在保护S.neurona中的关键作用由于Ifnγ ^-/-小鼠对S.神经元脑炎高度敏感，因此脑炎已得到充分证实。然而，文献中关于S.neurona疾病易感性在淋巴细胞缺陷小鼠中存在差异，缺乏 T 淋巴细胞及其相关的 Ifnγ 产生。在目前的研究中，我们调查了 2 种遗传不同的淋巴细胞缺失小鼠品系 C57Bl/6 (B6)对S. 神经元脑炎的易感性。scid和 Balb/c。.scid _ B6。scid小鼠被确定对S.neurona敏感脑炎，因为 100% 的受感染小鼠在感染后 60 天内 (DPI) 发展为神经系统疾病。巴尔布/c。scid小鼠几乎具有抗病性，因为只有 10% 的小鼠在 60 DPI 时出现神经系统疾病。脑炎在组织学上是可证实的，并且在从 B6 收集的小脑样本中发现了S. 神经元。scid但在 Balb/c 中不存在。scid老鼠。为了进一步研究 T 淋巴细胞衍生的 Ifnγ 的重要性，T 淋巴细胞被过继转移到 B6 中。scid老鼠。Ifnγ 感受态 T 淋巴细胞的过继转移提供了针对S.neurona的完全保护脑炎，但Ifnγ缺陷 T 淋巴细胞的转移没有 100% 的这些受体小鼠死于神经链球菌脑炎。收集的小脑样本的组织学分析证实了在发生神经系统疾病的受体小鼠中存在S.神经元和脑炎。这些研究表明，背景菌株对于研究 SCID 对S.neurona疾病的易感性至关重要，并表明产生 Ifnγ 的 T 淋巴细胞在S.neurona脑炎易感小鼠中具有保护作用。