CD 4 + T cell proliferation and inhibition of activation-induced cell death ( AICD ) in childhood asthma

Objective: The mechanism underlying immune inflammation and over-activation of T helper (Th) cells in childhood asthma was investigated through cell proliferation and activation-induced cell death (AICD) experiments. Methods: There were 30 children in the asthma group with an average age of 10.2 ± 3.1 years and 30 children in the normal control group with an average age of 10.5 ± 2.9 years. A cytometric bead array (CBA) was performed to detect Th1, Th2, and Th17 cytokines. After CD4+ T cells were separated using immunomagnetic beads and stimulated by phytohemagglutinin (PHA) combined with anti-CD3 antibodies in vitro, cell proliferation and AICD were analyzed. Finally, mRNA expression of the apoptosisand proliferation-related proteins Fas, FasL, and Bcl-2 was detected using quantitative polymerase chain reaction (PCR). Results: The serum cytokine levels of the children in the asthma group significantly increased compared to those of children in the normal control group (IL-4: 9.33 ± 2.25 ng/L vs. 4.59 ± 1.77 ng/L, P = 0.012; IL-10: 3.41 ± 0.80 ng/L vs. 1.36 ± 0.41 ng/L, P = 0.027; TNF: 7.63 ± 4.09 ng/L vs. 1.88 ± 0.52 ng/L, P = 0.023). The CD4+ T cell proliferation ability in the asthma group was significantly higher than that in the normal control group (OD450: 0.66 ± 0.14 vs. 0.28 ± 0.07, P<0.001), whereas the AICD rate was significantly lower than that in the normal control group (29.46 ± 5.25% vs. 60.11 ± 4.93%, P<0.001). The Fas mRNA expression in the CD4+ T cells from children in the asthma group was significantly decreased compared to that from the children in the normal control group, whereas the Bcl-2 expression was significantly higher than that from children in the normal control group. These differences were both statistically significant (P<0.001). Conversely, FasL expression did not differ (P > 0.05). Conclusion: Fas expression decreased and Bcl-2 expression increased in CD4+ T cells from the children in the asthma group, inhibiting AICD, and promoting proliferation of Th cells to some extent. Apoptosis inhibition and cell proliferation might result in over-activation of Th cells and aggravation of inflammatory infiltration in children with asthma.