Numerous studies report that changes in extracellular matrix components and receptors, such as CD44, contribute to immune cell recruitment and thus lesion formation in multiple sclerosis (MS).

In the present study, we used the cuprizone model to elucidate the expression pattern of CD44 in a toxin-induced MS model. Therefore, tissues of cuprizone-intoxicated mice were analyzed by real-time qRT-PCR and immunohistochemical staining against CD44. Co-localization analyses of CD44-positive cells with glial cell markers were performed by immunofluorescence labeling and in-situ hybridization. To investigate the functional importance of CD44 expression for myelination and glial cell activation, Cd44-deficient mice were used.

In this study we demonstrate that CD44 expression is induced in a time-dependent manner in an autoimmune-independent model of MS. Up-regulation of CD44 expression was primarily associated to the superficial and perivascular glia limitans and demyelinated white matter structures, particularly the corpus callosum. In the demyelinated corpus callosum, CD44 was localized on GFAP⁺ astrocytes and IBA1⁺ microglial cells. Despite a robust expression induction, Cd44-deficiency did not ameliorate cuprizone-induced pathology.

Although further studies will be needed to examine the functional relevance of CD44 in the cuprizone model, the spatial and temporal expression pattern of CD44 will pave the way to evaluate its precise role in different (immune and non-immune) pathological conditions.

许多研究报告说，细胞外基质成分和受体（如 CD44）的变化有助于免疫细胞募集，从而导致多发性硬化症 (MS) 中的病变形成。

在本研究中，我们使用铜宗模型来阐明 CD44 在毒素诱导的 MS 模型中的表达模式。因此，通过实时 qRT-PCR 和针对 CD44 的免疫组织化学染色分析了铜宗中毒小鼠的组织。CD44 阳性细胞与神经胶质细胞标记物的共定位分析通过免疫荧光标记和原位杂交进行。为了研究 CD44 表达对髓鞘形成和神经胶质细胞活化的功能重要性，使用了Cd44 缺陷小鼠。

在这项研究中，我们证明 CD44 表达在 MS 的自身免疫独立模型中以时间依赖性方式被诱导。CD44 表达的上调主要与浅表和血管周围神经胶质界限和脱髓鞘白质结构有关，尤其是胼胝体。在脱髓鞘胼胝体中，CD44 定位于 GFAP ⁺星形胶质细胞和 IBA1 ⁺小胶质细胞。尽管有强烈的表达诱导，但Cd44 缺乏并未改善铜宗诱导的病理学。

虽然需要进一步的研究来检查 CD44 在铜宗模型中的功能相关性，但 CD44 的时空表达模式将为评估其在不同（免疫和非免疫）病理条件下的精确作用铺平道路。