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Interleukin 4-Induced Gene 1 as an Emerging Regulator of B-Cell Biology and its Role in Cutaneous Melanoma.
Critical Reviews in Immunology ( IF 1.3 ) Pub Date : 2019-01-01 , DOI: 10.1615/critrevimmunol.2019030020
Armelle Prevost-Blondel 1 , Yolande Richard 1
Affiliation  

Interleukin 4 (IL4)-induced gene 1 (IL4I1) is an oxidase that degrades l-phenylalanine into phenylpyruvate, hydrogen peroxide, and ammonia. In contrast to other amino acid catabolic enzymes (i.e., indoleamine 2,3-dioxygenase and inducible nitric oxide synthase), IL4I1 is expressed not only in an intracellular form but also an active secreted form. Although about 20 yr ago IL4I1 was identified in murine B cells in response to IL4, we only recently established its key role in controlling B-cell receptor-mediated signaling during murine B-cell ontogeny and responses in physiological settings. Genetic IL4I1 invalidation increases the number of tumor-associated B cells and delays development of spontaneous metastatic melanoma in mice that are transgenic for the RET oncogene, without impairing tumor-specific antibody response. Although no consensus exists on phenotype and functions of melanoma-associated B cells, our results in RET mice argue for a protective role, with IL4I1 dampening this benefit. However, regulation of IL4I1 expression in innate-like and conventional B-cell subsets and its impact on B-cell properties are incompletely known, in particular, in cancer settings. This review aims to summarize our present knowledge of B cells in human and murine melanoma and address emerging questions about the impact of IL4I1 on B-cell functions in physiological and cancer settings. We note that during melanoma progression, IL4I1 may selectively be expressed by regulatory B cells and/or indirectly promote B-cell-mediated immunosuppression.

中文翻译:

白介素4诱导基因1作为B细胞生物学的新兴调节剂及其在皮肤黑色素瘤中的作用。

白介素4(IL4)诱导的基因1(IL4I1)是一种氧化酶,可将1-苯丙氨酸降解为苯丙酮酸,过氧化氢和氨水。与其他氨基酸分解代谢酶(即吲哚胺2,3-二加氧酶和诱导型一氧化氮合酶)相反,IL4I1不仅以细胞内形式表达,而且以活性分泌形式表达。尽管大约20年前在鼠B细胞中鉴定出对IL4有反应的IL4I1,但我们直到最近才确定其在鼠B细胞个体发育过程中控制B细胞受体介导的信号传导以及在生理环境中应答的关键作用。遗传性IL4I1无效会增加针对RET癌基因转基因的小鼠中与肿瘤相关的B细胞的数量,并延迟自发转移性黑色素瘤的发展,而不会损害肿瘤特异性抗体的应答。尽管在与黑色素瘤相关的B细胞的表型和功能上尚无共识,但我们在RET小鼠中的研究结果证明了其保护作用,IL4I1抑制了这种益处。但是,IL4I1表达在先天性和常规B细胞亚群中的调节及其对B细胞特性的影响尚不完全清楚,特别是在癌症环境中。这篇综述旨在总结我们目前在人类和鼠类黑色素瘤中对B细胞的了解,并探讨有关IL4I1对生理和癌症环境中B细胞功能的影响的新问题。我们注意到在黑色素瘤进展期间,IL4I1可能选择性地由调节性B细胞表达和/或间接促进B细胞介导的免疫抑制。IL4I1可以减轻这种益处。但是,IL4I1表达在先天性和常规B细胞亚群中的调节及其对B细胞特性的影响尚不完全清楚,特别是在癌症环境中。这篇综述旨在总结我们目前在人类和鼠类黑色素瘤中对B细胞的了解,并探讨有关IL4I1对生理和癌症环境中B细胞功能的影响的新问题。我们注意到在黑色素瘤进展期间,IL4I1可能选择性地由调节性B细胞表达和/或间接促进B细胞介导的免疫抑制。IL4I1可以减轻这种益处。但是,IL4I1在先天性和常规B细胞亚群中的表达调控及其对B细胞特性的影响尚不完全清楚,尤其是在癌症环境中。这篇综述旨在总结我们目前在人类和鼠类黑素瘤中对B细胞的了解,并探讨有关IL4I1对生理和癌症环境中B细胞功能的影响的新问题。我们注意到在黑色素瘤进展期间,IL4I1可能选择性地由调节性B细胞表达和/或间接促进B细胞介导的免疫抑制。这篇综述旨在总结我们目前在人类和鼠类黑素瘤中对B细胞的了解,并探讨有关IL4I1对生理和癌症环境中B细胞功能的影响的新问题。我们注意到在黑色素瘤进展期间,IL4I1可能选择性地由调节性B细胞表达和/或间接促进B细胞介导的免疫抑制。这篇综述旨在总结我们目前在人类和鼠类黑色素瘤中对B细胞的了解,并探讨有关IL4I1对生理和癌症环境中B细胞功能的影响的新问题。我们注意到在黑色素瘤进展期间,IL4I1可能选择性地由调节性B细胞表达和/或间接促进B细胞介导的免疫抑制。
更新日期:2019-11-01
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