CD4 and tuberculosis: Because IL-6 receptor (IL-6R) is mandatory for the bioactivity of IL-6 and we previously reported that down-regulation of IL-6R expression on CD4+ T cells by Mycobacterium tuberculosis is an important mechanism underlying reduced Th17 responses in patients with tuberculosis [24-26], we decided to investigate whether IL-6R expression is also correlated with Th17 responses in CHB patients.