Hepatitis B was still a worldwide health problem. This study aimed to conducted a systematic review and meta-analysis to assess a more precise estimation of factors that influence the response to hepatitis B vaccine in adults. Our included studies examined seroprotection rates close to the end of vaccination schedules in healthy adult populations. This meta-analysis including 21053 adults in 37 articles showed that a significantly decreased response to hepatitis B vaccine appeared in adults (age ≥ 40) (RR:1.86, 95% CI:1.55–2.23), male adults (RR:1.40, 95% CI:1.22–1.61), BMI ≥ 25 adults (RR:1.56, 95% CI:1.12–2.17), smoker (RR:1.53, 95% CI:1.21–1.93), and adults with concomitant disease (RR:1.39, 95% CI:1.04–1.86). Meanwhile, we further found a decreased response to hepatitis B vaccine appeared in adults (age ≥ 30) (RR:1.77, 95% CI:1.48–2.10), and adults (age ≥ 60) (RR:1.30, 95% CI:1.01–1.68). However, there were no difference in response to hepatitis B vaccine both in alcoholic (RR:0.90, 95% CI:0.64–1.26) and 0-1-12 vs. 0-1-6 vaccination schedule (RR:1.39, 95% CI:0.41–4.67). Pooling of these studies recommended the sooner the better for adult hepatitis B vaccine strategy. More vaccine doses, supplemental/additional strengthening immunity should be emphasized on the susceptible population of increasing aged, male, BMI ≥ 25, smoking and concomitant disease. The conventional 0-1-6 vaccination schedule could be still worth to be recommended.
The involvement of macrophages in Th17 responses is still poorly understood. While neutrophils are thought to be the predominant effector of Th17 responses, IL17 is also known to induce myelotropic chemokines and growth factors. Other T cell-derived cytokines induce nonclassical functions, suggesting that IL17 signaling may similarly elicit unique macrophage functions. We characterized the expression of subunits of the IL17 receptor on primary murine macrophages from different anatomical compartments. The greatest expression of IL17 receptors was observed on mucosal Ly6Chi “inflammatory” macrophages. We further observed upregulation of IL17 receptors in vitro on bone marrow-derived macrophages in response to peptidoglycan or CpG oligonucleotide stimuli, and in vivo, upon CFA administration. Macrophages expressing IL17 receptors were observed infiltrating the hearts of mice with myocarditis, and genetic ablation of IL17RA altered macrophage recruitment. Treating primary macrophages from a wide variety of different anatomic sources (as well as cell lines) with IL17A induced the production of unique profiles of cytokines and chemokines, including GM-CSF, IL3, IL9, CCL4/MIP1β and CCL5/RANTES. IL17A also induced production of IL12p70; IL17-signaling deficient macrophages elicited diminished IFNγ production by responding DO11.10 CD4+ cells when used as APCs. These data indicate that macrophages from different anatomic locations direct IL17-mediated responses.
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