Interleukin-1 abrogates anterior chamber-associated immune deviation.
Interleukin-1 abrogates anterior chamber-associated immune deviation.
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DOI：
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发表时间：
1990-10
影响因子：
4.4
通讯作者：
J. L. Benson;J. Niederkorn
中科院分区：
文献类型：
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作者：
J. L. Benson;J. Niederkorn
将同种异体抗原植入眼前房可诱导抗原特异性抑制全身性迟发性超敏反应(DTH)，并严重损害同种异体皮肤移植排斥反应。这种免疫改变的模式被称为前房相关免疫偏离(ACAID)，是导致眼前房内免疫豁免的潜在机制。以往的研究表明，与眼前房相关的免疫赦免可能是由于抗原呈递过程中白细胞介素2(IL-2)的缺乏所致。本研究探讨了IL-1在ACAID诱导中的作用。众所周知，将DBA/2肥大细胞瘤细胞(P815)腔内接种到同种异基因BALB/c受体体内，可导致抗原特异性的DTH反应抑制和肿瘤的进展。然而，作者发现，P388D1(DBA/2单核/巨噬细胞瘤)产生IL-1的亚系不仅不能在前房内进行性生长，而且能阻止DTH的抑制(P<0.01)。在IC接种P815细胞的研究中，证实了IL-1在消除ACAID中的作用。全身注射外源性IL-1(通过皮下微渗泵)可阻止接受P815细胞IC接种的宿主ACAID的诱导(P<0.01)。这些结果表明，ACAID的诱导以及前房的免疫特异性可能依赖于IC同种异体抗原处理过程中IL-1的缺乏。
Alloantigens placed into the anterior chamber of the eye elicit antigen-specific suppression of systemic delayed-type hypersensitivity (DTH) responses and severe impairment of skin allograft rejection. This pattern of immunologic alteration has been termed anterior chamber-associated immune deviation (ACAID) and is the underlying mechanism responsible for immunologic privilege within the anterior chamber of the eye. Previous studies indicate that the immunologic privilege associated with the anterior chamber of the eye might be the result of a deficiency of interleukin-2 (IL-2) during antigen presentation. The present study examined the role of IL-1 in the induction of ACAID. It is well known that intracameral (IC) inoculation of DBA/2 mastocytoma cells (P815) into allogeneic BALB/c recipients results in antigen-specific suppression of DTH responses and progressive tumor growth. The authors found, however, that sublines of P388D1 (DBA/2 monocyte/macrophage tumor) that produce IL-1 not only do not grow progressively in the anterior chamber, but also they can prevent the suppression of DTH (P less than or equal to 0.01). The role of IL-1 in the abolition of ACAID was confirmed in studies with IC-inoculated P815 cells. Systemic administration of exogenous IL-1 (by subcutaneous miniosmotic pumps) prevented the induction of ACAID in hosts that received IC inocula of P815 cells (P less than or equal to 0.01). These results indicate that induction of ACAID and perhaps the immune-privileged character of the anterior chamber is dependent on an IL-1 deficiency during the processing of IC alloantigens.