Detection of signaling pathways related to nuclear factor-κB in patients with psoriasis vulgaris using PCR-array analysis / 中华皮肤科杂志

Objective To detect the expression of 84 signaling molecules associated with nuclear factor-κB in lesions of Uygur patients with psoriasis.Methods Skin specimens were obtained from the lesional and paralesional skin of eight Uygur patients with psoriasis.Total RNA was extracted from the skin specimens and reversely transcribed into cDNA.PCR-array analysis was carried out to quantify the expressions of 84 signaling molecules related to nuclear factor-κB.Genes with a fold-change ＞ or =2 were defined as differentially expressed.Results Among the 84 tested genes,22 showed upregulated expression,7 downregulated expression,and the remaining 54 genes showed no significant changes in psoriatic lesions compared with the normal skin.The strongest upregulation was observed in the gene expressions of Caspase recruitment domain family 11 (CARD11) and granulocyte-macrophage colony-stimulating factor 2 (CSF2),and the most significant downregulation in the gene expression of interleukin 10 (IL-10),tumor necrosis factor superfamily member 5 (CD40) and nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor,epsilon (NFκBIE).Conclusion Multiple molecules involved in the NF-κB signaling pathway might be activated or inhibited in lesions of patients with psoriasis.

Caspase recruitment domain 11 and diffuse large B-cell lymphoma / 白血病·淋巴瘤

Diffuse large B-cell lymphoma (DLBCL) represents the most common type of malignant lymphoma. DLBCL is heterogeneous with respect to morphology, immunophenotype, biology, clinical presentation and outcome. Constitutive activity of the NF-κB pathway may contribute to the poor prognosis of patients with activated B cell-like (ABC) subgroup of DLBCL, caspase recruitment domain 11 (CARD11) is the important signal protein in the signaling pathway of NF-κB. Furthermore, various pre-clinical data have proved the importance of CARD11 in DLBCL. This review summarizes the biological characteristics of CARD11, and its relationship with NF-κB signaling transduction pathway and the outcome of DLBCL, so that we can better understanding the pathogenesis and new therapeutic target of DLBCL.