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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Dysregulated production of interleukin-10 (IL-10) and IL-12 by peripheral blood lymphocytes from human immunodeficiency virus-infected individuals is associated with altered proliferative responses to recall antigens.
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Dysregulated production of interleukin-10 (IL-10) and IL-12 by peripheral blood lymphocytes from human immunodeficiency virus-infected individuals is associated with altered proliferative responses to recall antigens.

机译：来自人类免疫缺陷病毒感染者的外周血淋巴细胞白细胞介素10（IL-10）和IL-12的生产失调与对召回抗原的增殖反应改变有关。

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The loss of immune function following infection with human immunodeficiency virus (HIV) may result from altered production of immunoregulatory cytokines such as interleukin-10 (IL-10) and IL-12. In this study, we analyzed IL-10 and IL-12 production by mitogen-stimulated peripheral blood mononuclear cells (PBMC) from HIV+ individuals and correlated their levels with proliferative responses to the recall antigens HIV p25 and influenza virus. We report two distinct groups of HIV+ patients. One group produced small amounts of IL-10, had PBMC that proliferated in response to recall antigens, and demonstrated enhanced recall antigen-induced proliferation upon addition of anti-IL-10 antibodies and/or IL-12. Conversely, the second group produced high levels of IL-10, had PBMC that failed to proliferate to recall antigens, and did not demonstrate enhanced proliferation upon addition of anti-IL-10 antibodies and/or IL-12. Mitogen-stimulated PBMC from both groups produced significantly lower levels of IL-12 than did those from HIV- controls. Analysis of the source of the IL-10-producing cell subset in PBMC demonstrated that in HIV+ individuals, IL-10 is produced by monocytes, while in HIV- controls, it is produced by both T cells and monocytes. Taken together, our results suggest that monocytes from HIV+ individuals secrete decreased amounts of IL-12, a Th1-type cytokine, which may lead to the development of Th2-type responses characterized by high IL-10 secretion and immune dysfunction.
机译：人类免疫缺陷病毒（HIV）感染后免疫功能的丧失可能是由于免疫调节细胞因子（如白介素10（IL-10）和IL-12）的产生改变所致。在这项研究中，我们分析了来自HIV +个体的有丝分裂原刺激的外周血单核细胞（PBMC）产生的IL-10和IL-12，并将其水平与对召回抗原HIV p25和流感病毒的增殖反应相关。我们报告了两组不同的HIV +患者。一组产生少量的IL-10，PBMC响应召回抗原而增殖，并在加入抗IL-10抗体和/或IL-12后证明召回抗原诱导的增殖增强。相反，第二组产生高水平的IL-10，PBMC不能增殖以召回抗原，并且在加入抗IL-10抗体和/或IL-12后未表现出增强的增殖。两组中受丝分裂刺激的PBMC产生的IL-12水平均显着低于HIV对照。对PBMC中产生IL-10的细胞亚群来源的分析表明，在HIV +个体中，IL-10是由单核细胞产生的，而在HIV-对照中，它是由T细胞和单核细胞产生的。两者合计，我们的结果表明，来自HIV +个体的单核细胞分泌的Th-1型细胞因子IL-12数量减少，这可能导致以IL-10分泌高和免疫功能异常为特征的Th2型反应的发展。

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