Rossol M, Häntzschel H, Wagner U
Medizinische Klinik und Poliklinik IV, Zentrum für Innere Medizin der Universität Leipzig, Liebigstr. 22, 04103, Leipzig, Germany.
Z Rheumatol. 2005 May;64(4):249-54. doi: 10.1007/s00393-005-0735-3.
Rheumatoid arthritis is characterized by a massive overproduction of monokines like TNFalpha, IL-6 and IL-1beta, which are predominantly produced by monocytes and macrophages. To date, the exact mechanisms of monocyte/macrophage activation have not been fully elucidated. One possible mechanism is their cell contact-dependent activation by activated T cells. The direct cell contact of monocytes/macrophages and T cells leads to an increased production of pro-inflammatory cytokines such as TNFalpha and IL-1beta. Stringent control of this mechanism by inhibitory factors appears mandatory under physiological conditions in order to avoid systemic cytokine release syndromes. The presence of inhibitory factors in the serum could represent such a mechanism. In healthy donors, apolipoprotein A-I was identified as such an inhibitory serum protein. In patients with rheumatoid arthritis, apolipoprotein A-I is found in decreased concentrations, possibly due to its role as a negative acute phase protein. The role of this and other inhibitory serum molecules are discussed.
类风湿性关节炎的特征是大量过度产生如肿瘤坏死因子α、白细胞介素-6和白细胞介素-1β等单核因子，这些因子主要由单核细胞和巨噬细胞产生。迄今为止，单核细胞/巨噬细胞激活的确切机制尚未完全阐明。一种可能的机制是它们被活化的T细胞通过细胞接触依赖性激活。单核细胞/巨噬细胞与T细胞的直接细胞接触会导致促炎细胞因子如肿瘤坏死因子α和白细胞介素-1β的产生增加。在生理条件下，似乎必须通过抑制因子对这种机制进行严格控制，以避免全身性细胞因子释放综合征。血清中存在抑制因子可能代表了这样一种机制。在健康供体中，载脂蛋白A-I被鉴定为这样一种抑制性血清蛋白。在类风湿性关节炎患者中，发现载脂蛋白A-I浓度降低，这可能是由于其作为负急性期蛋白的作用。本文讨论了这种及其他抑制性血清分子的作用。
