T-HELPER 2 INVOLVEMENT IN THE PATHOGENESIS OF BULLOUS PEMPHIGOID - ROLE OF SOLUBLE CD30 (SCD30)

Citation
O. Depita et al., T-HELPER 2 INVOLVEMENT IN THE PATHOGENESIS OF BULLOUS PEMPHIGOID - ROLE OF SOLUBLE CD30 (SCD30), Archives of dermatological research, 289(12), 1997, pp. 667-670
Citations number
27
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
03403696
Volume
289
Issue
12
Year of publication
1997
Pages
667 - 670
Database
ISI
SICI code
0340-3696(1997)289:12<667:T2IITP>2.0.ZU;2-Q
Abstract
Bullous pemphigoid (BP) is an autoimmune blistering skin disease in wh ich autoantibodies are directed against hemidesmosomal proteins of bas al keratinocytes, The presence of activated T helper cells in lesions and peripheral blood of BP patients, the eosinophilia, the high levels of serum IgE, eosinophil cationic protein and soluble immune products such as IL-2, sIL-2R, IL-5, soluble CD23 (sCD23) strongly suggest the involvement of a cell-mediated immune reaction in which Th2 lymphocyt es could play a pivotal role, To seek evidence to support this hypothe sis we evaluated serum levels of IL-4 and sCD30, a specific activation marker of cells able to produce Th2-like cytokines, in 25 patients af fected with BP, Serum from both healthy donors and pemphigus vulgaris (PV) patients were used as controls, Our results demonstrated signific antly higher levels of IL-4 and sCD30 in patients with BP in relation to both normal individuals (16.6 +/- 7.9 vs 4.5 +/- 2.2 pg/ml, P < 0.0 001; 30.3 +/- 10 vs 10.5 +/- 4 U/ml, P < 0.0001) and PV patients (6.2 +/- 4 pg/ml, P < 0.0001; 16 +/- 8.5 U/ml, P < 0.0001), Furthermore, a positive correlation between IL-4 and sCD30 was found (R = 0.85, P < 0 .0001), In a subset of seven patients observed after systemic immunosu ppressive therapy, we detected a significant reduction in sCD30 serum levels (36.9 +/- 7.3 vs 16.3 +/- 6.8 U/ml, P = 0.002), with a parallel improvement in their clinical condition, These results seem to be con sistent with the systemic involvement of Th2 lymphocytes in the pathog enesis of BP and suggest a role for sCD30 as a serological marker of d isease activity.