Lupu Andreea-Roxana, Cremer Lidia, Durbacă Steliana, Călugaru Ana, Herold Aurora, Kerek F, Szegli G, Radu D L
NIRDMI Cantacuzino, Bucharest-Romania.
Roum Arch Microbiol Immunol. 2006 Jan-Jun;65(1-2):59-65.
There are many studies demonstrating by different experimental models that non-steroidal antiinflammatory drugs (NSAIDs), also known as cyclooxygenase-2 (COX-2) inhibitors, can modulate immune response such as lymphoid cells differentiation and proliferation. There are experimental data which show that activated B cells can express mRNA COX-2, release prostaglandins (PGs) and produce immunoglobulins in PGs dependent manner. In this study, using different COX-2 inhibitors and applying personalized immunization scheme, we confirmed that it is possible to modulate in vivo antibody response against T cell dependent antigens, substantiating the importance of PGE2 and E prostanoid receptor (EP-R) in antibody generation. Our results point out the fact that we must be more careful when we apply vaccines containing T-cell dependent antigens, such as tetanus or diphteric anatoxin, to the patients under an intense antiinflammatory treatment.
有许多研究通过不同的实验模型表明，非甾体抗炎药（NSAIDs），也称为环氧化酶-2（COX-2）抑制剂，可以调节免疫反应，如淋巴细胞的分化和增殖。有实验数据表明，活化的B细胞可以表达COX-2 mRNA，释放前列腺素（PGs）并以PGs依赖的方式产生免疫球蛋白。在本研究中，我们使用不同的COX-2抑制剂并应用个性化免疫方案，证实了在体内调节针对T细胞依赖性抗原的抗体反应是可能的，这证实了PGE2和前列环素受体（EP-R）在抗体产生中的重要性。我们的结果指出，当我们给正在接受强化抗炎治疗的患者接种含有T细胞依赖性抗原的疫苗（如破伤风或白喉类毒素）时，必须更加谨慎。
