title: Infections as triggers and complications of systemic lupus erythematosus.
abstract: A growing body of experimental and clinical evidence supports the pivotal role of infections in the induction or exacerbation of systemic lupus erythematosus (SLE). Infections can be responsible for aberrant immune response leading to a loss of tolerance towards native proteins. Molecular mimicry, especially between Sm or Ro autoantigens and EBV Nuclear Antigen-1 response, as well as the over-expression of type 1 INF genes are among the major contributors to SLE development. On the other hand infections are very common in SLE patients, where they are responsible for 30-50% of morbidity and mortality. Several factors, either genetic, including complement deficiencies or mannose-binding lectin deficiency or acquired such as severe disease manifestations or immunosuppressant use, predispose SLE patients to infections. All types of infections, including bacterial, viral and opportunistic infections, have been reported and the most frequently involved sites of infections are the same as those observed in the general population, including respiratory, skin, and urinary tract infections. Some preventive measures could be adopted in order to reduce the rate of infections in SLE patients: i.e. screening for Mycobacterium tuberculosis and for some chronic viral infections before immunosuppressive treatment; adequate prophylaxes or drug adjustments when indicated, and pneumococcal and influenza vaccinations in patients with stable disease.
authors.affiliation: Division of Rheumatology, Department of Clinical and Experimental Medicine, University of Padova, Italy. adoria@unipd.it
authors.forename: A
authors.initials: A
authors.lastname: Doria
authors.forename: M
authors.initials: M
authors.lastname: Canova
authors.forename: M
authors.initials: M
authors.lastname: Tonon
authors.forename: M
authors.initials: M
authors.lastname: Zen
authors.forename: E
authors.initials: E
authors.lastname: Rampudda
authors.forename: N
authors.initials: N
authors.lastname: Bassi
authors.forename: F
authors.initials: F
authors.lastname: Atzeni
authors.forename: S
authors.initials: S
authors.lastname: Zampieri
authors.forename: A
authors.initials: A
authors.lastname: Ghirardello
mesh_terms: D002908:Chronic Disease; D019309:Epstein-Barr Virus Nuclear Antigens / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007108:Immune Tolerance; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007239:Infections / Q000209:etiology* / Q000276:immunology; D007252:Influenza Vaccines; D007251:Influenza, Human / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000401:mortality; D008403:Mass Screening; D018716:Molecular Mimicry; D009169:Mycobacterium tuberculosis; D022242:Pneumococcal Vaccines; D012261:Ribonucleoproteins / Q000276:immunology / Q000378:metabolism; D055517:snRNP Core Proteins / Q000276:immunology / Q000378:metabolism; D000099207:SS-A Antigen
chemical_list: D019309:Epstein-Barr Virus Nuclear Antigens; D007166:Immunosuppressive Agents; D007252:Influenza Vaccines; D022242:Pneumococcal Vaccines; D012261:Ribonucleoproteins; D055517:snRNP Core Proteins; D000099207:SS-A Antigen