Abnormal expression of CD43 in patients with systemic lupus erythematosus and its clinical significance.
Chin Med J (Engl)
; 125(7): 1266-71, 2012 Apr.
Article
en En
| MEDLINE
| ID: mdl-22613599
BACKGROUND: Previous studies indicate that CD43 plays a role in regulating the adhesion of lymphocytes, cell mutation and activation, however, little is known about its effect on systemic lupus erythematosus (SLE). This study was designed to explore the clinical significance of CD43 in SLE patients. METHODS: We used microarray and real-time PCR to detect the mRNA and protein expression of magnetic bead sorted T cells and B cells from peripheral blood mononuclear cells (PBMCs) of SLE patients, and analyzed the relationship between CD43 and the clinical indexes. RESULTS: Both microarray and real-time PCR results showed that CD43 mRNA was significantly decreased in PBMCs of SLE patients compared with healthy controls (P < 0.001). There were no significant differences between lupus nephritis and non-lupus nephritis patients, and neuropsychiatric and non-neuropsychiatric patients. CD43 mRNA expression was significantly reduced in T cells but not in B-cells in SLE patients compared to healthy controls (P < 0.01). Compared with healthy controls, the percentage of CD43(+) cells in the PBMCs of SLE was significantly decreased (P = 0.004), and the CD43 fluorescence intensity in CD3(+)/CD43(+) cells and CD19(+)/CD43(+) cells was also significantly weaker than in healthy controls (P = 0.039 and 0.003). There was no significant difference in the percentage of CD3(+)/CD43(+) cells, CD19(+)/CD43(+) cells between the two groups. The CD43 fluorescence intensity in CD3(+)/CD43(+) cells was inversely correlated with the levels of IgG and IgM (r = -0.8 and -0.6). CONCLUSIONS: Compared to healthy controls, both CD43 mRNA and protein expressions were reduced in T cells from patients with SLE, and were inversely correlated with IgG.
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Banco de datos:
MEDLINE
Asunto principal:
Leucosialina
/
Lupus Eritematoso Sistémico
Límite:
Humans
Idioma:
En
Año:
2012
Tipo del documento:
Article