Soluble Interleukin 2 Receptor and Interleukin 1α in Toxic Epidermal Necrolysis: A Comparative Analysis of Serum and Blister Fluid Samples | Allergy and Clinical Immunology | JAMA Dermatology | JAMA Network
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1.
Roujeau  JCStern  R Severe adverse cutaneous reactions to drugs.  N Engl J Med. 1994;3311272- 1285Google ScholarCrossref
2.
Roujeau  JCChosidow  OSaiag  PGuillaume  JC Toxic epidermal necrolysis (Lyell syndrome).  J Am Acad Dermatol. 1990;231039- 1958Google ScholarCrossref
3.
Palmares  JCorreia  ODelgado  LVaz-da-Silva  MMesquita-Guimarães  JCastro-Correia  J Ocular involvement in toxic epidermal necrolysis.  Ocul Immunol Inflamm. 1993;1171- 177Google ScholarCrossref
4.
Paul  CWolkenstein  PAdle  H  et al.  Apoptosis as a mechanism of keratinocyte death in toxic epidermal necrolysis.  Br J Dermatol. 1996;134710- 714Google ScholarCrossref
5.
Viard  IWehrli  PBullani  R  et al.  Inhibition of toxic epidermal necrolysis by blockage of CD95 with human intravenous immunoglobulin.  Science. 1998;282490- 493Google ScholarCrossref
6.
Hertl  MGeisel  JBoecker  CMerk  HF Selective generation of CD8+ T-cell clones from the peripheral blood of patients with cutaneous reactions to beta-lactam antibiotics.  Br J Dermatol. 1993;128619- 626Google ScholarCrossref
7.
Mauri-Hellweg  DBettens  FMauri  DBrander  CHuntziker  TPichler  WJ Activation of drug-specific CD4+ and CD8+ T cells in individuals allergic to sulfonamides, phenytoin, and carbamazepine.  J Immunol. 1995;155462- 472Google Scholar
8.
Schnyder  BFrutig  KMauri-Hellweg  DLimat  AYawalkar  NPichler  WJ T-cell–mediated cytotoxicity against keratinocytes in sulfamethoxazole-induced skin reaction.  Clin Exp Allergy. 1998;281412- 1417Google ScholarCrossref
9.
Yawalkar  NEgli  FHari  YNievergelt  HBraathen  LRPichler  WJ Infiltration of cytotoxic T cells in drug-induced cutaneous eruptions.  Clin Exp Allergy. 2000;30847- 855Google ScholarCrossref
10.
Miyauchi  HHosokawa  HAkaeda  TIba  HAsada  Y T-cell subsets in drug-induced toxic epidermal necrolysis: possible pathogenic mechanism induced by CD8-positive T cells.  Arch Dermatol. 1991;127851- 855Google ScholarCrossref
11.
Villada  GRoujeau  JCClérici  TBourgault  IRevuz  J Immunopathology of toxic epidermal necrolysis.  Arch Dermatol. 1992;12850- 53Google ScholarCrossref
12.
Correia  ODelgado  LRamos  JPResende  CFleming-Torrinha  JA Cutaneous T-cell recruitment in toxic epidermal necrolysis: further evidence of CD8+ lymphocyte involvement.  Arch Dermatol. 1993;129466- 468Google ScholarCrossref
13.
Le Cleach  LDelaire  SBoumsell  L  et al.  Blister fluid T lymphocytes during toxic epidermal necrolysis are functional cytotoxic cells which express human natural killer (NK) inibitory receptors.  Clin Exp Immunol. 2000;119225- 230Google ScholarCrossref
14.
Bastuji-Garin  SRzany  BStern  RShear  NHNaldi  LRoujeau  JC Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson and erythema multiforme.  Arch Dermatol. 1993;12992- 96Google ScholarCrossref
15.
Moore  NBiour  MPaux  G  et al.  Adverse drug reaction monitoring: doing it in the French way.  Lancet. 1985;21056- 1058Google ScholarCrossref
16.
Leyva  LTorres  MJPosadas  S  et al.  Anticonvulsant-induced toxic epidermal necrolysis: monitoring the immunologic response.  J Allergy Clin Immunol. 2000;105157- 165Google ScholarCrossref
17.
Kuziel  WAGreene  WC Interleukin-2 and the IL-2 receptor: new insights into structure and function.  J Invest Dermatol. 1990;94 (6, suppl) 27S- 32SGoogle ScholarCrossref
18.
Jobin  NGarrel  DBernier  J Increased serum-soluble interleukin-2 receptor in burn patients: characterization and effects on the immune system.  Hum Immunol. 2000;61233- 246Google ScholarCrossref
19.
Rubin  LAKurman  CCFritz  ME  et al.  Soluble interleukin-2 receptors are released from activated human lymphoid cells in vitro.  J Immunol. 1985;1353172- 3177Google Scholar
20.
Teodorczyk-Injeyan  JSparkes  BGMills  GBFalk  REPeters  WJ Increase of serum interleukin 2 receptor level in thermally injured patients.  Clin Immunol Immunopathol. 1989;51205- 215Google ScholarCrossref
21.
Symons  JAWood  NCGiovine  FSDuff  GW Soluble IL-2 receptor in rheumatoid arthritis: correlation with disease activity: IL-1 and IL-2 inhibition.  J Immunol. 1988;1412612- 2618Google Scholar
22.
Miyamoto  TAkashi  KHayashi  S  et al.  Serum concentration of the soluble interleukin-2 receptor for monitoring acute graft-versus-host disease.  Bone Marrow Transplant. 1996;17185- 190Google Scholar
23.
Robertson  MJRitz  J Biology and clinical relevance of human natural killer cells.  Blood. 1990;762421- 2438Google Scholar
24.
Fehniger  TABluman  EMPorter  MM  et al.  Potential mechanisms of human natural killer cell expansion in vivo during low-dose IL-2 therapy.  J Clin Invest. 2000;106117- 124Google ScholarCrossref
25.
Murphy  JERobert  CKupper  TS Interleukin-1 and cutaneous inflammation: a crucial link between innate and acquired immunity.  J Invest Dermatol. 2000;114602- 608Google ScholarCrossref
26.
Kupper  TSDeitch  EABaker  CCWong  W The human burn wound as a primary source of interleukin-1 activity.  Surgery. 1986;100409- 415Google Scholar
27.
Hauser  CSaurat  JHSchmitt  AJaunin  FDayer  JM Interleukin 1 is present in normal human epidermis.  J Immunol. 1986;1363317- 3323Google Scholar
28.
Yu  TKCaudell  EGSmid  CGrimm  EA IL-2 activation of NK cells: involvement of MKK1/2/ERK but not p38 kinase pathway.  J Immunol. 2000;1646244- 6251Google ScholarCrossref
29.
Stepkowski  SMKirken  RA Specific suppression of interleukin 2 biosynthesis by synthetic antisense oligodeoxynucleotides does not influence allograft rejection.  Transplantation. 2000;692480- 2483Google ScholarCrossref
30.
Symington  FWSantos  EB Lysis of human keratinocytes by allogeneic HLA class-I specific cytotoxic T cells: keratinocytes ICAM-1 (CD54) and T cell LFA-1 (CD11a/CD18) mediate enhanced lysis of INF-γ-treated keratinocytes.  J Immunol. 1991;1462169- 2175Google Scholar
Study
January 2002

Soluble Interleukin 2 Receptor and Interleukin 1α in Toxic Epidermal Necrolysis: A Comparative Analysis of Serum and Blister Fluid Samples

Author Affiliations

From the Department of Dermatology, Instituto Português Oncologia (Dr Correia), and Department of Immunology, Faculty of Medicine (Drs Correia, Delgado, and Fleming-Torrinha), Porto, Portugal; and Department of Dermatology, Hôpital Henri Mondor, Université Paris XII, Créteil, France (Drs Roujeau and Le Cleach).

Arch Dermatol. 2002;138(1):29-32. doi:10.1001/archderm.138.1.29
Abstract

Background  Toxic epidermal necrolysis (TEN) is a rare but severe adverse drug disease, characterized by extensive skin and mucosal detachment with participation of different immunoinflammatory pathways, in particular with early participation of activated CD8+ T lymphocytes.

Objective  To further study the potential role of T lymphocytes in the early phase of keratinocyte necrosis.

Design  Prospective study.

Setting  University hospitals.

Patients  Thirteen patients with clinical and histopathologic criteria of TEN and 6 patients with second-degree burns.

Main Outcome Measures  Measurement of soluble interleukin (IL) 2 receptor (sIL-2R) and IL-1α in serum samples and fluid of recent blisters.

Results  In the blister fluid of patients with TEN, we found significantly higher levels of sIL-2R than in patients with burns, whereas IL-1α levels were higher in the blister fluid of burned patients. No significant differences were found in serum samples of patients with TEN and burns, in either sIL-2R or IL-1α. In TEN we also found significantly higher levels of sIL-2R in the blister fluid compared with serum samples, pointing to a predominantly local production contrasting with the low concentration of sIL-2R in the blister fluid of burned patients.

Conclusions  Our findings of elevated sIL-2R levels in blister fluid of patients with TEN are probably related to a local down-regulation of an immunologically mediated cytotoxic reaction and further support the involvement of activated T lymphocytes in the early blisters of TEN.

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