title: [Immunosuppression and infection in transplant recipients].
abstract: Recognizing a foreign element is an inherent characteristic of living beings and guarantees their survival. Evading this defense mechanism is one of the most difficult requirements for transplant success, but it leads to a series of consequences, mainly related to infection. T lymphocytes are the cornerstone of the allogenic response. These cells recognize intracellular and extracellular antigens over HLA molecules in host cells. As a consequence, lymphocytic expansion occurring on several levels is produced, and a humoral or cellular response is the final result. The immunosuppression regimens used in transplantation include induction, maintenance and rescue therapy. Induction therapy serves primarily to decrease the proportion of T-cell precursors and to lower the efficacy of antigen presentation. With respect to maintenance therapy, cyclosporine and tacrolimus inhibit cytokine transcription, azathioprine, and mycophenolate mofetil inhibit nucleotide synthesis, and sirolimus and everolimus inhibit transduction of growth factor signals. As a consequence of immunosuppression, opportunistic microorganisms may appear with endogenic reactivation of latent infection or from an exogenous origin. Prevention of these infections by proper knowledge of the risk factors, rapid diagnosis, and adequate management are fundamental to guarantee the survival of the patient.
authors.affiliation: Servicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, Madrid, España.
authors.forename: Pilar
authors.initials: P
authors.lastname: Martín-Dávila
authors.forename: Marino
authors.initials: M
authors.lastname: Blanes
authors.forename: Jesús
authors.initials: J
authors.lastname: Fortún
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D065095:Calcineurin Inhibitors; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D016867:Immunocompromised Host; D007166:Immunosuppressive Agents / Q000009:adverse effects* / Q000145:classification / Q000494:pharmacology; D017053:Infection Control; D007239:Infections / Q000209:etiology*; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis / Q000235:genetics; D009181:Mycoses / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D009894:Opportunistic Infections / Q000209:etiology / Q000517:prevention & control; D016377:Organ Transplantation; D010272:Parasitic Diseases / Q000209:etiology; D011183:Postoperative Complications / Q000209:etiology* / Q000517:prevention & control; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology; D014181:Transplantation Immunology
chemical_list: D065095:Calcineurin Inhibitors; D016207:Cytokines; D007166:Immunosuppressive Agents; D036341:Intercellular Signaling Peptides and Proteins; D019384:Nucleic Acid Synthesis Inhibitors