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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Reversible lacrimal gland-protective regulatory T-cell dysfunction underlies male-specific autoimmune dacryoadenitis in the nonobese diabetic mouse model of Sjogren syndrome
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Reversible lacrimal gland-protective regulatory T-cell dysfunction underlies male-specific autoimmune dacryoadenitis in the nonobese diabetic mouse model of Sjogren syndrome

机译：可逆性泪腺保护性调节性T细胞功能障碍是Sjogren综合征非肥胖糖尿病小鼠模型中雄性特异性自身免疫性泪腺炎的基础

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CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells are required to maintain immunological tolerance; however, defects in specific organ-protective Treg cell functions have not been demonstrated in organ-specific autoimmunity. Non-obese diabetic (NOD) mice spontaneously develop lacrimal and salivary gland autoimmunity and are a well-characterized model of Sjogren syndrome. Lacrimal gland disease in NOD mice is male-specific, but the role of Treg cells in this sex-specificity is not known. This study aimed to determine if male-specific autoimmune dacryoadenitis in the NOD mouse model of Sjogren syndrome is the result of lacrimal gland-protective Treg cell dysfunction. An adoptive transfer model of Sjogren syndrome was developed by transferring cells from the lacrimal gland-draining cervical lymph nodes of NOD mice to lymphocyte-deficient NOD-SCID mice. Transfer of bulk cervical lymph node cells modelled the male-specific dacryoadenitis that spontaneously develops in NOD mice. Female to female transfers resulted in dacryoadenitis if the CD4(+)CD25(+) Treg-enriched population was depleted before transfer; however, male to male transfers resulted in comparable dacryoadenitis regardless of the presence or absence of Treg cells within the donor cell population. Hormone manipulation studies suggested that this Treg cell dysfunction was mediated at least in part by androgens. Surprisingly, male Treg cells were capable of preventing the transfer of dacryoadenitis to female recipients. These data suggest that male-specific factors promote reversible dysfunction of lacrimal gland-protective Treg cells and, to our knowledge, form the first evidence for reversible organ-protective Treg cell dysfunction in organ-specific autoimmunity.
机译：需要CD4（+）CD25（+）Foxp3（+）调节性T（Treg）细胞来维持免疫耐受。但是，尚未在器官特异性自身免疫中证实特定器官保护性Treg细胞功能的缺陷。非肥胖型糖尿病（NOD）小鼠自发地产生泪腺和唾液腺自身免疫，是Sjogren综合征的一个特征鲜明的模型。 NOD小鼠的泪腺疾病是雄性特异性的，但是尚不知道Treg细胞在这种性别特异性中的作用。这项研究旨在确定干燥综合征的NOD小鼠模型中的雄性特异性自身免疫性泪腺炎是否是泪腺保护性Treg细胞功能障碍的结果。通过将细胞从NOD小鼠的泪腺引流子宫颈淋巴结转移至淋巴细胞缺乏的NOD-SCID小鼠，建立了Sjogren综合征的过继转移模型。大量颈淋巴结细胞的转移模拟了在NOD小鼠中自发发展的雄性特异性泪腺炎。如果富含CD4（+）CD25（+）Treg的人群在转移前被消耗掉，则女性间的转移会导致泪腺炎。然而，无论供体细胞群中是否存在Treg细胞，雄性至雄性转移均导致类似的泪腺炎。激素操纵研究表明，这种Treg细胞功能异常至少部分是由雄激素介导的。令人惊讶的是，雄性Treg细胞能够阻止泪腺炎转移至雌性受体。这些数据表明，男性特异性因子可促进泪腺保护性Treg细胞的可逆功能障碍，并且据我们所知，是器官特异性自身免疫中可逆性器官保护性Treg细胞功能障碍的第一个证据。

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