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Since the discovery of ABO blood types, there has been mounting evidence of the association between blood types and infectious diseases. However, so far, there is rarely available research about the potential role of ABO blood types in haemorrhagic fever with renal syndrome (HFRS) infection. Our aim was to investigate the relationship between ABO blood types and the development of HFRS infection in Qingdao, China. We carried out a retrospective study enrolling 116 HFRS patients as the case group and 373 healthy subjects as the control group. ABO blood type distribution was analysed using the Chi-square test and logistic regression analysis. Results showed that the distribution of ABO blood types between the two groups was significantly different (X2 = 18.151, P < 0.05). Blood type B was less frequently observed [odds ratio (OR), 0.404; confidence interval (CI), 0.238–0.684; P < 0.01], while blood type AB was more frequently observed in the case group (OR, 2.548; CI, 1.427–4.549; P < 0.01). Since significantly more males were affected than females, we further analysed the data by gender as well as blood types and obtained consistent results for males. Our findings indicated that populations with blood type AB might be more prone to HFRS infection, whereas those with blood type B might be less susceptible to HFRS infection, which will help to make risk stratification in infection control.

Background Autoimmune hemolytic anemia (AIHA), a life-threatening anemia with rapid onset, is caused by autoantibody directed to self red blood cells (RBCs). Currently, mechanisms underlying AIHA pathogenesis are largely undefined. Here we explored the correlation of IL-33 with AIHA disease activity and evaluated IL-33 based therapeutics in AIHA treatment. Methods Thirty patients diagnosed with AIHA of warm-type autoantibodies without treatment were enrolled and followed up for 6 months. Levels of cytokines including IL-33, IL-4, IL-6 and IL-13 was determined with ELISA. AIHA disease activity was presented by levels of reticulocyte count, hemoglobin and lactate dehydrogenase. Serum RBC-bound IgG autoantibody was detected using anti-IgG antibody with flow cytometry. To evaluate the effect of IL-33 blockade on AIHA development, groups of B6 mice were immunized with rat RBCs plus recombinant IL-33 protein or IL-33 neutralizing antibody respectively and detected for levels of anti-RBC antibody, frequency of reticulocytes and destruction of transfused syngeneic mouse RBCs. Results Serum level of IL-33 was higher in AIHA patients compared with healthy individuals. Of interest, serum IL-33 was positively correlated with AIHA disease activity and sensitive to their changes in AIHA patients under clinical management. Mechanistically, IL-33 could promote the production of anti-RBC autoantibody. Serum IL-33 was closely associated with serum anti-RBC autoantibody and sensitive to their changes in AIHA patients. Accordingly, blockade of IL-33 interfered with AIHA incidence and ameliorated disease activity. Vice vasa, enforced IL-33 promoted AIHA incidence and disease activity. Conclusions IL-33 was a potential biomarker for monitoring disease activity and therapeutic response in AIHA patients. Targeting IL-33 was a promising strategy for controlling autoantibody production in AIHA patients. Electronic supplementary material The online version of this article (doi:10.1186/s12967-015-0745-0) contains supplementary material, which is available to authorized users.

Additional file 1: Figures. Gating strategy for anti-RBC antibody analysis, serum levels of sST2 in AIHA patients, Th2 cytokines in AIHA mice co-injected with IL-33 protein or IL-33 neutralizing antibody, B cell response to IL-33 stimulation or IL-33 blockade, and effect of IL-6 on IL-33-mediated autoantibody production were presented.