Increased CD4+ T cell infiltrates in rheumatoid arthritis–associated interstitial pneumonitis compared with idiopathic interstitial pneumonitis

Objective

To study lymphocyte markers in rheumatoid arthritis (RA)–associated interstitial pneumonitis (IP) compared with idiopathic IP.

Methods

Paraffin‐embedded lung biopsy specimens from patients with RA (n = 15) and from those without RA (n = 16), all of whom had a diagnosis of either nonspecific IP or usual IP, were studied. Tissue sections from each patient were reviewed by a pathologist, who was blinded to the clinical data. Age and pulmonary function test results were similar in RA and non‐RA patients. After high‐temperature antigen unmasking, sections were incubated with mouse monoclonal antibodies directed against CD3, CD4, CD8, CD16, and CD20. All slides were coded, and digital images (100× magnification) of the entire tissue area were obtained. Staining was quantified using computer‐assisted image analysis.

Results

Staining for CD4 was more prominent in patients with RA than in the non‐RA comparison group (median 9.3 cells/mm², interquartile range [IQR] 5.5–27.3 versus 0.6 cells/mm², IQR 0.2–1.9; P = 0.002). CD4+ cell counts were increased in RA patients with nonspecific IP as well as in RA patients with usual IP, with no major difference between these groups. Results were similar for quantification of CD3 (P = 0.012). There was a less striking trend toward more CD8+ cells in RA patients (P = 0.27 versus those with non‐RA lung disease).

Conclusion

IP lesions in patients with RA are characterized by an increased number of CD4+ cells, as compared with that in patients with idiopathic IP. This finding suggests that CD4+ T cells are critical for the development of pulmonary manifestations in RA, and may have implications for the treatment of RA‐associated lung disease.

     

黄芪总黄酮对扑热息痛所致肝损伤的防护机理探讨

目的 :研究黄芪总黄酮对扑热息痛所致肝损伤的防护机理。方法 :用高压液相测定扑热息痛及代谢产物和苯巴比妥诱导睡眠模型研究黄芪总黄酮 (TFA)对扑热息痛的代谢及TFA抗扑热息痛所致损伤的机理。结果 :TFA可明显降低尿中硫醚胺酸的浓度 ,其变化与TFA浓度成反比 ;但对其它代谢产物的影响无明显统计学差异。苯巴比妥诱导小鼠睡眠实验结果显示 ,TFA (10 0mg·kg^-1)本身对苯巴比妥代谢无明显影响 (P>0 .05) ,扑热息痛 (400mg·kg^-1)可显著延长小鼠的睡眠时间 (P<0.001) ;但TFA (100mg·kg^-1)明显缩短扑热息痛所延长的苯巴比妥诱导的睡眠时间 (P<0.005)。结论 :TFA抗扑热息痛损伤的作用机理可能与TFA抑制扑热息痛某些代谢过程以及降低扑热息痛代谢过程中产生毒性代谢产物有关。