Introduction: HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic progressive myelopathy associated with an inflammation of the central nervous system (CNS), being characterized by perivascular infiltration of inflammatory cells. HTLV-1-infected cells have the capacity to migrate through endothelial layers by enhancing adhesion receptor expression and corresponding ligands. T cells interact with the extracellular matrix via integrin receptors and these interactions affect both cell migration and proliferation. The importance of these interactions in retrovirus-induced diseases, however, remains less clear. Methods: Herein we studied the expression of 3 integrin alpha chains (CD49d, CD49e, and CD49f) on the membrane of T-cell subsets in patients infected by HTLV-1, both HAM/TSP patients and oligo/asymptomatic subjects who were asymptomatic or presented slight manifestations related to the virus infection. Results: We observed higher peripheral blood frequency of CD49d^hiCD4⁺ and CD49d^hiCD8⁺ T cells in HTLV-1-infected patients. Conclusion: Our findings suggest that the increased expression of adhesion molecules, such as CD49d on T lymphocytes from HTLV-1-infected patients may contribute to the pathogenesis of the disease, in both oligo/asymptomatic and HAM/TSP-infected subjects. Accordingly, it is conceivable that there is a potential use of CD49d as target for a therapeutic approach aiming at blocking migration of activated T cells from HTLV-1-infected patients into the CNS, thus avoiding the progression to HAM/TSP.
Neuroimmunomodulation

中文翻译：

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CD49d 在来自 HTLV-1 感染患者的循环 T 淋巴细胞中上调。

简介： HTLV-1 相关脊髓病/热带痉挛性下肢轻瘫 (HAM/TSP) 是一种慢性进行性脊髓病，与中枢神经系统 (CNS) 炎症相关，其特征是血管周围炎症细胞浸润。HTLV-1 感染的细胞具有通过增强粘附受体表达和相应配体迁移通过内皮层的能力。T 细胞通过整合素受体与细胞外基质相互作用，这些相互作用影响细胞迁移和增殖。然而，这些相互作用在逆转录病毒引起的疾病中的重要性仍不清楚。方法：在此，我们研究了 HTLV-1 感染的患者，包括 HAM/TSP 患者和无症状或表现出轻微与病毒感染有关的表现。结果：我们观察到HTLV-1 感染患者的 CD49d ^hi CD4 ⁺和 CD49d ^hi CD8 ⁺ T 细胞的外周血频率较高。结论：我们的研究结果表明，粘附分子的表达增加，例如来自 HTLV-1 感染患者的 T 淋巴细胞上的 CD49d，可能有助于该疾病的发病机制，无论是在寡聚/无症状还是 HAM/TSP 感染的受试者中。因此，可以想象，CD49d 作为治疗方法的靶点是有潜在用途的，该方法旨在阻止激活的 T 细胞从 HTLV-1 感染患者迁移到 CNS，从而避免进展为 HAM/TSP。
神经免疫调节