Background: Cystic fibrosis is mainly caused by a genetic mutation, through a gene located on chromosome 7.The result of all mutations is decreased chloride secretion and, consequently, increased reabsorption of sodium in the cell space.The disease occurs as a cascade effect following infection and the subsequent inflammatory process.The most common bacteria that cause endobronchial infection are Staphylococcus aureus and Pseudomonas aeruginosa.Methodology: Amino acid sequences of autoantigens for cystic fibrosis were selected from the AAgAtlas autoantigen database (http://biokb.ncpsb.org/aagatlas/).The amino acid sequence of each autoantigen was used as input in PSI-BLAST (https://blast.ncbi.nlm.nih.gov/Blast.cgi) to find similar antigens of pathogens associated with infection in cystic fibrosis.For epitope prediction, the autoantigens analyzed in this study were used as entry for the Ellipro server (http://tools.iedb.org/ellipro/).Results: Autoantigens ADRBK2 (Uniprot code: P35626), GAD1 (Uniprot code: Q99259), GAD2 (Uniprot code: Q05329), HSPD1 (Uniprot code: P10809), SLC30A8 (Uniprot code: Q8IWU4).and SLC33A1 (Uniprot code: O00400).were retrieved from AAgAtlas.The Ellipro tool predicted several possible cross-reactive epitopes between autoantigens and bacterial antigens (Table 1; Figure 123456). Conclusion:Bacterial antigens that mimic the autoantigens involved in Cystic Fibrosis have been identified, suggesting that there is a relationship between infections and the development of this disease or the development of bacterial resistance, which could explain the etiology in some patients.