Details

Autor(en) / Beteiligte

• Wong, Chun K
• Wong, Purple T. Y
• Tam, L. S
• Li, Edmund K
• Chen, D. P
• Lam, Christopher W. K

Titel

Activation Profile of Intracellular Mitogen-Activated Protein Kinases in Peripheral Lymphocytes of Patients with Systemic Lupus Erythematosus

Ist Teil von

• Journal of clinical immunology, 2009-11, Vol.29 (6), p.738-746

Ort / Verlag

Boston: Boston : Springer US

Erscheinungsjahr

2009

Quelle

SpringerLink

Beschreibungen/Notizen

• Introduction Systemic lupus erythematosus (SLE) is a systemic autoimmune disease associated with aberrant activation of T and B lymphocytes. Abnormal activation of intracellular signaling molecules in lymphocytes by inflammatory cytokines can instigate the inflammation in SLE. Materials and Methods The activation of extracellular signal-regulated kinase (ERK), c-Jun NH₂-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) in inflammatory cytokine IL-18-activated monocytes, CD4+ T helper (Th) lymphocytes, CD8+ T lymphocytes, and CD19+B lymphocytes in 22 SLE patients and 20 sex- and age-matched control subjects were measured by flow cytometry. Results and Discussion The basal expressions of phospho-p38 MAPK in CD4+ T lymphocytes, CD8+ T lymphocytes, and B lymphocytes were significantly higher in SLE patients than controls (all p < 0.05). The expression of phospho-p38 MAPK in CD4+ T lymphocytes, CD8+ T lymphocytes and B lymphocytes, and phospho-JNK in CD8+ T lymphocytes and B lymphocytes was also significantly elevated in SLE patients upon the activation by IL-18, exhibiting significant correlation with the plasma concentrations of Th1 chemokine CXCL10 (all p < 0.05). The expression of phospho-JNK in IL-18 activated CD8+ T lymphocytes and the relative % fold increase of the expression of phospho-JNK upon IL-18 activation in B lymphocytes were significantly correlated with SLE disease activity index (both p < 0.05). Conclusion The inflammation-mediated activation of JNK and p38 MAPK signaling pathways in T and B lymphocytes can be the underlying intracellular mechanisms causing lymphocyte hyperactivity in SLE.