African health sciences · 2019
Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis.
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Zahid Shakoor, Mustafa Adam, Dina Assiri, Sawsan Bakry, Felwa AlMarshad, Mohammed GadElRab, Hasan Abdulaziz
Аннотация
BACKGROUND: Persistent antigenic stimulation due to repeated exposure to nickel may lead to chronic inflammation resulting in allergic contact dermatitis (ACD).
OBJECTIVES: This study was performed to assess nickel induced immune activation among patients sensitized against nickel.
PATIENTS AND METHODS: A total of 35 patients (29 females and 6 males; mean age 36±9 years) with nickel contact dermatitis and 20 patch test negative healthy individuals (14 females and 6 males; mean age 29±7 years) were included in this study. Peripheral blood of patients and controls was incubated with nickel sulfate for 24 hours. Immune activation was assessed by CD69 up-regulation on T lymphocyte sub-sets by flow cytometry.
RESULTS: Base line expression of CD69 on CD8+ lymphocytes was higher among patients compared to controls (4.1±1.3%vs2.8±1.1%;p<0.009). There was no difference in proportions of CD±CD69+ cells between patients and controls (3.2±0.9%vs2.3±0.8%). Exposure to nickel induced expression of CD69 on a significantly higher proportion of CD4+ lymphocytes (22.1±6.2%) of the ACD patients compared to controls (2.8±2.5%;p<0.0001). Similarly nickel induced CD69 expression on a higher proportion of CD8+ lymphocytes (18.2±5.3%) from ACD patients compared to the controls (1.9±1.8%;p<0.0006).
CONCLUSION: CD69 molecule appears to be an important regulator of immune response in nickel contact dermatitis.
OBJECTIVES: This study was performed to assess nickel induced immune activation among patients sensitized against nickel.
PATIENTS AND METHODS: A total of 35 patients (29 females and 6 males; mean age 36±9 years) with nickel contact dermatitis and 20 patch test negative healthy individuals (14 females and 6 males; mean age 29±7 years) were included in this study. Peripheral blood of patients and controls was incubated with nickel sulfate for 24 hours. Immune activation was assessed by CD69 up-regulation on T lymphocyte sub-sets by flow cytometry.
RESULTS: Base line expression of CD69 on CD8+ lymphocytes was higher among patients compared to controls (4.1±1.3%vs2.8±1.1%;p<0.009). There was no difference in proportions of CD±CD69+ cells between patients and controls (3.2±0.9%vs2.3±0.8%). Exposure to nickel induced expression of CD69 on a significantly higher proportion of CD4+ lymphocytes (22.1±6.2%) of the ACD patients compared to controls (2.8±2.5%;p<0.0001). Similarly nickel induced CD69 expression on a higher proportion of CD8+ lymphocytes (18.2±5.3%) from ACD patients compared to the controls (1.9±1.8%;p<0.0006).
CONCLUSION: CD69 molecule appears to be an important regulator of immune response in nickel contact dermatitis.