American Journal of Immunology

Interplay of Cytokines and Chemokines in the Pathogenesis of Systemic Lupus Erythematosus

Dilip Shah, Ajay Wanchu and Archana Bhatnagar

DOI : 10.3844/ajisp.2011.29.38

American Journal of Immunology

Volume 7, Issue 3

Pages 29-38


Problem statement: Dysbalance of T-helper-cell (Th) cytokines and chemokines was suggested to contribute to the pathogenesis of Systemic Lupus Erythematosus (SLE). Recent reports suggest the involvement of cytokines and chemokines in the pathogenesis of SLE, but their relationship with each other and particularly in the severity of disease, was not yet understood. We analyzed the interaction between cytokines and chemokines and their relationship with severity of disease in SLE. Approach: Serum levels of cytokines and chemokines were determined by ELISA and severity of disease were measured by by using SLE Disease Activity Index (SLEDAI) score. Results: The serum levels of cytokine (IL-2, IFN-γ, IL-6, IL-10 and IL-12) and chemokine (CCL2, CCL5 and CXCL10) were variably associated with disease activity in SLE patients. Strict interaction between cytokines and chemokines was observed in SLE patients. Interleukin-6 was positively correlated with CCL5 while IL-12 was also analogous correlated with CXCL10 in SLE patients. The kidney involvement in SLE patients was related with intense increased levels of cytokines (IFN-γ, IL-12) and chemokines (CCL2, CCL5 and CXCL10). Conclusion: These data suggest that interplay of cytokines and chemokines may be involved in the severity of disease. Also, a better understanding of the cytokines and chemokines interaction may likely to provide important clues to the pathogenic mechanism and pave the way toward more effective therapeutics.


© 2011 Dilip Shah, Ajay Wanchu and Archana Bhatnagar. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.