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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Activated human B lymphocytes express cyclooxygenase-2 and cyclooxygenase inhibitors attenuate antibody production.
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Activated human B lymphocytes express cyclooxygenase-2 and cyclooxygenase inhibitors attenuate antibody production.

机译：活化的人B淋巴细胞表达环氧合酶2，而环氧合酶抑制剂减弱抗体的产生。

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摘要

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for the treatment of inflammatory diseases and target cyclooxygenases 1 and 2 (Cox-1, Cox-2) that are responsible for PG production. Newer Cox-2-selective drugs have been heavily prescribed to quench inflammation. Little is known about whether or not these drugs influence human B lymphocytes and their ability to produce Ab. We report herein that activated human B cells not only highly express Cox-2 and produce PGs, but that the NSAID indomethacin and Cox-2-selective drugs profoundly inhibit the ability of human B cells to produce IgG and IgM in vitro. Human blood B cells highly express Cox-2 mRNA and protein and produce PGs after activation with CD40L, pansorbin, or CD40L plus BCR engagement. Cox-2 is also highly expressed by human tonsil B cells, as shown by immunohistochemistry. Cox-inhibiting drugs modestly affect purified B cell proliferation but profoundly reduce Ab production. The ability of whole blood to produce IgM and IgG followingstimulation is also strongly inhibited. In support that Cox-2 plays a seminal role in B lymphocyte Ab production, Cox-2 knockout mice have 64% less IgM and 35% less IgG than normal littermate controls. These findings support that NSAIDs and the new Cox-2-selective drugs have an unsuspected target, the B cell, and attenuate Ab production in humans. Use of NSAIDs may therefore influence autoantibody production in autoimmune diseases and may dampen humoral immunity in response to antigenic challenge/vaccination.
机译：非甾体类抗炎药（NSAIDs）被广泛用于治疗炎症性疾病和负责产生PG的目标环氧合酶1和2（Cox-1，Cox-2）。已经大量开出了新的Cox-2选择性药物来猝灭炎症。这些药物是否影响人类B淋巴细胞及其产生Ab的能力知之甚少。我们在此报道，活化的人B细胞不仅高度表达Cox-2并产生PG，而且NSAID消炎痛和Cox-2选择性药物深刻地抑制了人B细胞在体外产生IgG和IgM的能力。人血B细胞通过CD40L，pansorbin或CD40L加上BCR激活后，高表达Cox-2 mRNA和蛋白质并产生PG。免疫组织化学显示，Cox-2在人扁桃体B细胞中也高度表达。抑制Cox的药物会适度影响纯化的B细胞增殖，但会大大降低Ab的产生。全血在刺激后产生IgM和IgG的能力也被强烈抑制。为了支持Cox-2在B淋巴细胞Ab产生中发挥重要作用，与正常同窝仔对照相比，Cox-2敲除小鼠的IgM和IgG降低了64％。这些发现支持NSAID和新的Cox-2选择性药物具有意想不到的靶标B细胞，并减弱了人类的Ab产生。因此，使用NSAID可能会影响自身免疫疾病中自身抗体的产生，并可能会因应抗原激发/接种而减弱体液免疫。

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