**5. Conclusions**

L5 may contribute to atherosclerosis by augmenting macrophage foam cell formation, upregulating CD11c expression, or enhancing the expression of inflammatory mediators, such as IL-6, IL-8, and TNF-α. These findings provide new insight into the pathogenesis of increased CVD risk in RA that cannot be explained by conventional risk factors.

#### **Supplementary Materials:** Supplementary materials can be found at http://www.mdpi.com/1422-0067/21/16/ 5883/s1.

**Author Contributions:** C.-K.C. conceived and designed the study, performed the data analysis, drafting and revising of the manuscript. P.-K.C. conceived the study, acquired the data, and performed the data analysis. J.-L.L., S.-H.C. and T.-Y.H. performed the clinical assessment, obtained clinical data, and carried out statistical analysis. P.-J.L. conceived the study and collected clinical data. C.-H.C. generated the original hypothesis and revised the manuscript. D.-Y.C. conceived and designed the study, generated the original hypothesis, acquired the clinical data, performed the data analysis, and revised the manuscript. All authors have read and agreed to the published version of the manuscript.

**Funding:** This work was supported by a grant from China Medical University Hospital (DMR-108-184), and by a grant (MOST 107-2314-B-039-053-MY3) from the Ministry of Science and Technology, Taiwan.

**Acknowledgments:** The authors thank Shiow-Jiuan Wey, of Chung Shan Medical University Hospital, Taiwan, and Rebecca Bartow, of the Texas Heart Institute, Houston, USA, for editorial assistance. The microscope image was performed in the Medical Research Core Facilities, Office of Research & Development at China medical University, Taiwan.

**Conflicts of Interest:** The authors declare no conflict of interest.
