Tumor necrosis factor alpha regulation of immunoglobulin secretion in trauma patients.

Circulatory shock Pub Date : 1994-05-01
J A Teodorczyk-Injeyan, M Cembrzynska-Nowak, S Lalani, S Rizoli, G Taylor
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Abstract

Major trauma-related immune dysfunction is observed at the time of augmented release of immunopathologic mediators. In the present study, T cell-dependent immunoglobulin (Ig) synthesis in peripheral blood mononuclear cell (PBMC) cultures from blunt trauma patients (N = 12, injury severity score (ISS) 27-50), was reduced by 30- > 90%. This coincided with significantly (P < 0.001-0.01) elevated secretion of the biologically active tumor necrosis factor alpha (TNF alpha). Modulation of the TNF alpha activity by anti-TNF alpha antibody (anti-TNF alpha Ab) led to dose-dependent alterations in IgG synthesis. IgG production increased (up to 300%) in cultures treated with 0.5-2 micrograms/ml of the antibody, where low levels of TNF alpha activity often persisted. However, immunoglobulin synthesis was eradicated in preparations exposed to higher concentrations (10 micrograms/ml) of anti-TNF alpha Ab and devoid of TNF alpha biological activity. The treatment with anti-TNF alpha Ab had no effect on mitogen- or alloantigen-induced PBMC proliferation. Thus, in severely traumatized patients, biological activities of endogenous TNF alpha may include modulation of T cell-dependent B lymphocyte function. Immunoregulatory potential of TNF alpha should, therefore, be considered in therapeutic strategies to abrogate its activity.

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肿瘤坏死因子α对创伤患者免疫球蛋白分泌的调节作用。
主要的创伤相关免疫功能障碍是在免疫病理介质释放增强时观察到的。在本研究中,钝性创伤患者(N = 12,损伤严重程度评分(ISS) 27-50)外周血单个核细胞(PBMC)培养物中的T细胞依赖性免疫球蛋白(Ig)合成降低了30- > 90%。这与生物活性肿瘤坏死因子α (TNF α)分泌显著(P < 0.001-0.01)升高相吻合。抗TNF α抗体(抗TNF α Ab)对TNF α活性的调节导致IgG合成的剂量依赖性改变。在0.5-2微克/毫升抗体处理的培养物中,IgG的产生增加(高达300%),其中低水平的TNF α活性通常持续存在。然而,暴露于较高浓度(10微克/毫升)的抗TNF α Ab和缺乏TNF α生物活性的制剂中,免疫球蛋白合成被根除。抗tnf α Ab治疗对有丝分裂原或同种异体抗原诱导的PBMC增殖无影响。因此,在严重创伤患者中,内源性TNF α的生物活性可能包括T细胞依赖性B淋巴细胞功能的调节。因此,在治疗策略中应考虑TNF α的免疫调节潜力,以消除其活性。
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