INDUCTION OF CUTANEOUS LYMPHOCYTE-ASSOCIATED ANTIGEN EXPRESSION BY GROUP-A STREPTOCOCCAL ANTIGENS IN PSORIASIS

Citation
Bs. Baker et al., INDUCTION OF CUTANEOUS LYMPHOCYTE-ASSOCIATED ANTIGEN EXPRESSION BY GROUP-A STREPTOCOCCAL ANTIGENS IN PSORIASIS, Archives of dermatological research, 289(12), 1997, pp. 671-676
Citations number
20
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
03403696
Volume
289
Issue
12
Year of publication
1997
Pages
671 - 676
Database
ISI
SICI code
0340-3696(1997)289:12<671:IOCLAE>2.0.ZU;2-N
Abstract
The cutaneous lymphocyte-associated antigen (CLA) has been proposed as a homing receptor for the selective migration of memory T cells into the skin. To investigate the effect of group A streptococci (GAS) on t he migration of T cells in psoriasis, CLA expression was assessed by d ouble-staining for CD3 and the HECA-452 epitope on peripheral blood T cells from 13 patients with psoriasis, 10 patients with other inflamma tory skin diseases and 12 normal controls before and after 7 days cult ure with a GAS sonicate, Candida albicans (control antigen) or medium. In addition, CLA(+), and CLA(-), CD3(+) CD45RO(+) subsets were isolat ed from individuals in each group and V beta 2 expression and prolifer ation to GAS studied. Mean CLA expression by freshly isolated T cells was almost identical in the three groups. After culture with GAS, T ce lls from the psoriatic patients and control groups showed a significan t increase in mean percentage CLA(+) expression compared to medium (P < 0.002, P < 0.05, respectively). This induction was inhibited by the addition of anti-IL-12 antibody. However, in psoriatic patients, but n ot in controls, the GAS-induced increase was significantly greater tha n that of C. albicans (P < 0.002) and was accompanied by a decrease in T cells positive for the peripheral lymph node homing receptor, L-sel ectin (P < 0.05). The percentage of V beta 2(+) T cells was markedly h igher in the CLA(+) than in the CLA-T-cell subset in psoriatic patient s (P < 0.01) and controls; both subsets proliferated to GAS, in each g roup. These findings suggest a differential modulation of specific tis sue homing receptors on T cells by GAS in psoriasis.