Zong Yuan, Kamoi Koju, Ando Naoko, Kurozumi-Karube Hisako, Ohno-Matsui Kyoko
Department of Ophthalmology and Visual Science, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Front Microbiol. 2022 Jun 2;13:738742. doi: 10.3389/fmicb.2022.738742. eCollection 2022.
Human T-cell lymphotropic virus type 1 (HTLV-1) was the first retrovirus identified as the causative agent of human diseases, such as adult T-cell leukemia, HTLV-1-associated myelopathy, and HTLV-1 uveitis (HU). HU is one of the most frequent ocular inflammatory diseases in endemic areas, which has raised considerable public health concerns. Approximately 30% of HU patients develop secondary glaucoma, which is higher than the general uveitis incidence. We therefore investigated the mechanism underlying the high incidence of glaucoma secondary to HU After contact with HTLV-1-producing T cells (MT-2), human trabecular meshwork cells (HTMCs) were infected. The infected cells increased in number, and nuclear factor (NF)-κB expression was activated. Contact between MT-2 cells and HTMCs resulted in significantly upregulated production of inflammatory cytokines, such as IL-6, and chemokines, such as CXCL10, CCL2, and CXCL-8. These findings indicate that the mechanism underlying secondary glaucoma in HU may involve proliferation of trabecular meshwork tissue after contact with HTLV-1-infected cells, resulting in decreased aqueous humor outflow. Upregulated production of inflammatory cytokines and chemokines simultaneously disrupts the normal trabecular meshwork function. This mechanism presumably leads to increased intraocular pressure, eventually resulting in secondary glaucoma.
人类嗜T细胞病毒1型（HTLV-1）是首个被鉴定为人类疾病病原体的逆转录病毒，这些疾病包括成人T细胞白血病、HTLV-1相关脊髓病以及HTLV-1葡萄膜炎（HU）。HU是流行地区最常见的眼部炎性疾病之一，这引发了相当大的公共卫生关注。大约30%的HU患者会继发青光眼，这一比例高于一般葡萄膜炎的发病率。因此，我们研究了HU继发青光眼高发的潜在机制。在与产生HTLV-1的T细胞（MT-2）接触后，人小梁网细胞（HTMCs）被感染。被感染的细胞数量增加，核因子（NF）-κB表达被激活。MT-2细胞与HTMCs之间的接触导致炎性细胞因子如IL-6以及趋化因子如CXCL10、CCL2和CXCL-8的产生显著上调。这些发现表明，HU继发青光眼的潜在机制可能涉及与HTLV-1感染细胞接触后小梁网组织的增殖，从而导致房水流出减少。炎性细胞因子和趋化因子产生的上调同时破坏了正常的小梁网功能。这种机制大概会导致眼压升高，最终引发继发青光眼。
