Kaplan-Meier analysis of combined DSA and autoantibody status showed a trend to worse BOS free survival but did not meet statistical significance. the presence of autoantibodies did not correlate with increase in the incidence or severity of PGD. The prevalence of donor specific antibodies (DSA) in the entire cohort was 73%, with an increased prevalence of DSA noted in the autoantibody positive group (78.7% vs. 54.5%) than in the autoantibody negative group. BOS was observed in 20% of the cohort, with a median time to onset of 291 days post-transplant. Patients with pre-transplant autoantibodies experienced a statistically significant decrease in BOS-free survival (p=0.029 by log-rank test). CONCLUSIONS: In our cohort, we CDKN2B observed a high prevalence of autoantibodies and DSA in lung transplant recipients. Pre-transplant autoantibodies were associated with de novo development of Stattic DSA along with a decrease in BOS-free survival. Limitations to our study include the small sample size and single center enrollment, along with limited time for follow-up. autoantibodies after lung transplantation and 9 among10 developed DSA as well. Open in a separate window Physique 1. Enrollment and presence of autoantibodies In comparing the autoantibody positive and negative groups, with the exception of age at transplant, there were no significant differences in baseline characteristics between the two groups. In our cohort, autoantibody positive patients were transplanted at a more youthful age compared to those without autoantibodies (54.513.7 years vs. 63.55.8 years, p=0.0043). While there was no significant difference in autoantibody status based on the underlying diagnosis for transplant, it is worth noting that all patients in our cohort with IPF and CF were autoantibody positive (Table 1, p=0.05). Table 1. Baseline Characteristics comparing groups with and without autoantibodies. autoantibodies post-transplant. Table 2: Outcomes C Autoantibody Subgroups: Pre-transplant Positive vs Pre-transplant Negative DSA that develop after lung transplantation experienced higher prevalence of BOS (p=0.002). Pre-transplant HLA antibodies did not impact graft function and in most cases HLA antibodies detected before transplantation disappeared after transplantation. However, Kauke et al did not evaluate non-HLA antibodies. In our study, we statement that recipients with pre-transplant (non-HLA) autoantibodies (Col I, Col V and K1T) not only experienced higher prevalence of DSA but also those who developed DSA experienced higher concentration of autoantibodies and were less likely to obvious them (autoantibodies) post-transplant. Saini et al (24) analyzed serum from lung transplant patients who developed DSA. DSA were detectable on an average 3 months post-transplant and antibodies to Col IV and K1T developed following DSA. In addition, autoantibodies persist despite DSA clearance. Our findings in our study suggest Stattic pre-transplant autoantibodies especially at higher concentration in DSA positive group. We believe that recipients with alloantibodies and autoantibodies may have higher levels of blood circulation pro-inflammatory cytokines as exhibited by Tiriveedhi et al (15). This might result in a self-perpetuating process leading to antibody binding to uncovered new epitopes after ischemia reperfusion injury. Antigen-antibody binding prospects to complement activation Stattic which can then damage epithelial cell surface by match mediated cytotoxicity as explained in a mouse model by Patel et al (27). 5.3. Autoantibodies before and after lung transplantation. Our study evaluated the effect of traditional immunosuppression on autoantibodies. Several of those who experienced pre-transplant autoantibodies did not obvious post-transplant (17/23; 73%) with the traditional immunosuppression strategy. About 22% (n=10) percentage also developed autoantibodies post-transplant. Group with pre-transplant autoantibodies experienced less BOS free survival. Our findings suggest preexisting autoantibodies play a role in graft injury after lung transplantation and we speculate that these preexisting Stattic autoantibodies might be involved in underlying cause of chronic lung disease. Current methods of immunosuppression seem to have minimal impact on their clearance. Those autoantibodies that develop post-transplant may be associated with DSA and did not seem to be associated as strongly with BOS. PGD was observed in 34% of our cohort, however the presence of autoantibodies (including pre-transplant autoantibodies) was not shown to increase the incidence or severity of PGD. Our results differ from previously published studies (9, 15) and may be attributable to differences in sample size, titer of antibodies and their synergy. However, the role of humoral immunity in main graft dysfunction.