title: Altered calcium influx of peripheral Th2 cells in pediatric Crohn's disease: infliximab may normalize activation patterns.
abstract: OBJECTIVE
  Crohn's disease is a chronic inflammation of the gastrointestinal tract with an abnormal immune phenotype. We investigated how intracellular calcium kinetics of Th1 and Th2 lymphocytes alter upon specific inhibition of Kv1.3 and IKCa1 channels in pediatric Crohn's disease.
  
  
  METHODS
  Blood was taken from 12 healthy and 29 Crohn's disease children. Of those, 6 were switched to infliximab and re-sampled after the 4th infliximab treatment. Intracellular calcium levels were monitored using flow cytometry in the presence or absence of specific inhibitors of Kv1.3 and IKCa1 potassium channels.
  
  
  RESULTS
  In Crohn's disease treated with standard therapy, calcium response during activation was higher than normal in Th2 cells. This was normalized in vitro by inhibition of Kv1.3 or IKCa1 potassium channels. After the switch to infliximab, potassium channel function and expression in Th2 lymphocytes were comparable to those in Th1 cells.
  
  
  CONCLUSIONS
  These results may indicate that potassium channels are potential immune modulatory targets in Crohn's disease.
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.|Department of Dietetics and Nutrition Sciences, Faculty of Health Sciences, Semmelweis University, Budapest, Hungary.
authors.forename: Csaba
authors.initials: C
authors.lastname: Orbán
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.
authors.forename: Dolóresz
authors.initials: D
authors.lastname: Szabó
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.
authors.forename: Anna
authors.initials: A
authors.lastname: Bajnok
authors.affiliation: Department of Laboratory Medicine, Semmelweis University, Budapest, Hungary.
authors.forename: Barna
authors.initials: B
authors.lastname: Vásárhelyi
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.|MTA-SE, Pediatrics and Nephrology Research Group, Budapest, Hungary.
authors.forename: Tivadar
authors.initials: T
authors.lastname: Tulassay
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.|MTA-SE, Pediatrics and Nephrology Research Group, Budapest, Hungary.
authors.forename: András
authors.initials: A
authors.lastname: Arató
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.|MTA-SE, Pediatrics and Nephrology Research Group, Budapest, Hungary.
authors.forename: Gábor
authors.initials: G
authors.lastname: Veres
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.|MTA-SE, Pediatrics and Nephrology Research Group, Budapest, Hungary.
authors.forename: Gergely
authors.initials: G
authors.lastname: Toldi
mesh_terms: D000293:Adolescent; D002118:Calcium / Q000378:metabolism*; D002648:Child; D003424:Crohn Disease / Q000188:drug therapy / Q000378:metabolism*; D005260:Female; D005765:Gastrointestinal Agents / Q000627:therapeutic use*; D006801:Humans; D000069285:Infliximab / Q000627:therapeutic use*; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D015221:Potassium Channels / Q000187:drug effects; D018418:Th2 Cells / Q000187:drug effects / Q000378:metabolism*
chemical_list: D005765:Gastrointestinal Agents; D015221:Potassium Channels; D000069285:Infliximab; D002118:Calcium
keywords: Crohn’s disease; IKCa1; Immune response; Immunity; Immunology and Microbiology Section; Kv1.3; Th2; infliximab