Panayi G S, Mills M M
Rheumatol Int. 1986;6(1):25-9. doi: 10.1007/BF00270661.
The AMLR (autologous mixed lymphocyte reaction) was performed in 24 control subjects, 41 patients with rheumatoid arthritis (RA), 19 patients with ankylosing spondylitis (AS), and 7 patients with psoriatic arthritis (PSA). It was found to be depressed in 21 of the RA subjects and this was linked to medication with sodium aurothiomalate or D-penicillamine. Addition of ultrapure interleukin 1 (IL-1), indomethacin, or catalase did not cause any improvement in the AMLR but some improvement was noted in those RA patients with subnormal AMLR when pure, recombinant interleukin 2 (IL-2) was added to the cultures. Since autoreactive T-cells are generated during the AMLR which are capable of providing help for immunoglobulin production, it is proposed that the defective AMLR seen after second-line drug treatment may be the mechanism whereby rheumatoid factor (RF) production is down-regulated during such treatment.
对24名对照受试者、41名类风湿性关节炎（RA）患者、19名强直性脊柱炎（AS）患者和7名银屑病关节炎（PSA）患者进行了自体混合淋巴细胞反应（AMLR）。发现21名RA受试者的AMLR受到抑制，这与金硫代苹果酸钠或D-青霉胺用药有关。添加超纯白细胞介素1（IL-1）、消炎痛或过氧化氢酶并未使AMLR有任何改善，但当向培养物中添加纯的重组白细胞介素2（IL-2）时，那些AMLR低于正常水平的RA患者有了一些改善。由于在AMLR过程中会产生能够为免疫球蛋白产生提供帮助的自身反应性T细胞，因此有人提出，二线药物治疗后出现的有缺陷的AMLR可能是类风湿因子（RF）在这种治疗期间产生下调的机制。
