Lima, João Paulo Matos SantosPatrocínio, Helmut Kennedy Azevedo do2021-09-272021-10-062021-09-272021-10-062021-04-20PATROCÍNIO, Helmut Kennedy Azevedo do. Investigação in silico de epítopos de proteínas do sistema nervoso periférico para o entendimento da síndrome de Guillain-Barré desencadeada pelo vírus Epstein-Barr. 2021. 60 f. Monografia (Graduação em Biomedicina) – Universidade Federal do Rio Grande do Norte, Natal, 2021.https://repositorio.ufrn.br/handle/123456789/43248Guillain-Barré Syndrome (SGB) is an autoimmune disease caused by an immune response against autoantigens of the peripheral nervous system (PNS). Most SGB immunopathology studies have investigated the cross-reaction between myelin sheath ganglioside antigens and carbohydrates from the bacterium Campylobacter jejuni. However, SGB has a spectrum of subtypes and, particularly, the form of Inflammatory Acute Demyelinating Polyradiculoneuropathy (AIDP) has little evidence of a relationship with C. jejuni or autoimmunity against gangliosides. In this work, we used the literature search strategy and search in biological databases to select SNP myelin sheath proteins and Epstein-Barr virus immunogenic proteins, as well as Human Leukocyte Antigens (HLAs) associated with the AIDP subtype. Computational tools were also used to predict HLA ligands, predict cytokine production and homology analysis between anchoring nonapeptides. The anchoring nonapeptides of the EBV proteins and myelin proteins were compared for homology in at least four TCR-binding residues, because this is the average amount of contacts between the TCR and the peptide. The selection condition was that a residue must be located in position P5, at least one in positions P2 or P8 and the rest in P3, P4, P6 or P7. According to these criteria, four proteins (MAG, MBP, Periaxin and P0) have peptides that have homology with EBV peptides. Prediction of cytokine production showed that some pairs of homologous peptides are stimulators of cytokines interleukin 4 (IL-4) or Interferongamma (IFN-γ) or both, which is indicative of the ability to activate a cell response T helper 1 (Th1) or T helper 2 (Th2).Síndrome de Guillain-BarréPolirradiculoneuropatia Aguda Desmielinizante InflamatóriaMimetismo molecularReação cruzadaInteração pMHC-TCRGuillain-Barre syndromeAcute Inflammatory Demyelinating PolyradiculoneuropathyMolecular mimicryCross reactionpMHC-TCR interaction.bachelorThesis