title: Expression of the skin-homing receptor in peripheral blood lymphocytes from subjects with nonimmediate cutaneous allergic drug reactions.
abstract: BACKGROUND
  In nonimmediate cutaneous reactions to drugs, the skin is the organ most frequently involved, and T cells may play a relevant role. T cells related to skin immune responses express the cutaneous lymphocyte-associated antigen (CLA), the skin-homing receptor.
  
  
  METHODS
  We studied the expression of the CLA in peripheral blood T cells from nine subjects with exanthematous reactions induced by beta-lactams (4), phenytoin (2), propyphenazone (1), spiramycin plus metronidazol (1), and captopril plus tiazide (1). The cutaneous symptoms appeared at least 6 h after drug intake. CLA expression was evaluated by flow cytometry at the time of the reaction (T1) and 1 month later (T2). HLA-DR activation marker expression was also evaluated at T1. In four patients, it was necessary to readminister the culprit drug to establish a causal relationship, and sequential estimation of the markers was performed. Two control groups were included: healthy controls and subjects exposed to the culprit drugs with good tolerance. Values were compared by nonparametric statistics.
  
  
  RESULTS
  The expression of circulating CLA + T cells at T1 was increased compared to healthy controls (median = 20.4 vs 9.4) (P < 0.001), and the patients also expressed increased levels of HLA-DR (median = 3.8) (P < 0.005). Comparison between T1 and T2 (median = 11.2) also showed differences in levels of CLA+ T cells (P < 0.01). The patients re-exposed to the culprit drug showed an increase followed by a decrease of circulating CLA+ T cells (P < 0.05) and CLA+ HLA-DR+ (P < 0.05) paralleling the symptoms.
  
  
  CONCLUSIONS
  These data support the immunologic nature of delayed skin reactions to drugs, and suggest that these CLA+ T cells parallel the disease evolution and may participate in the pathophysiologic mechanisms.
authors.affiliation: Allergy Service, La Paz Hospital, Madrid, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Blanca
authors.forename: S
authors.initials: S
authors.lastname: Posadas
authors.forename: M J
authors.initials: MJ
authors.lastname: Torres
authors.forename: L
authors.initials: L
authors.lastname: Leyva
authors.forename: C
authors.initials: C
authors.lastname: Mayorga
authors.forename: L
authors.initials: L
authors.lastname: Gonzalez
authors.forename: C
authors.initials: C
authors.lastname: Juarez
authors.forename: J
authors.initials: J
authors.lastname: Fernández
authors.forename: L F
authors.initials: LF
authors.lastname: Santamaria
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D004342:Drug Hypersensitivity / Q000276:immunology*; D005076:Exanthema / Q000276:immunology*; D005260:Female; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis*; D008875:Middle Aged; D051381:Rats; D016201:Receptors, Lymphocyte Homing / Q000032:analysis*; D013601:T-Lymphocytes / Q000737:chemistry*
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; C063419:CTAGE1 protein, human; D006684:HLA-DR Antigens; D008562:Membrane Glycoproteins; D016201:Receptors, Lymphocyte Homing