Human HSP 60 peptide responsive T cell lines are similarly present in both Behçet's disease patients and healthy controls.

Heat shock protein (HSP, 60/65 kDa) is investigated as a candidate autoantigen in Behçet's disease (BD), a systemic vasculitis of unknown origin, and a prominent response to 'disease-specific epitopes' of mycobacterial and human HSP60/65 is described in BD patients. In this study, long-term T cell lines from peripheral blood of BD patients (n=6) and controls (n=7) were stimulated with mycobacterial recombinant HSP and purified protein derivate (PPD) and expanded with IL-2. In the BD group, 15 out 27 and in the controls, 25 out of 35 PPD specific T cell lines have responded to the synthetic peptides of the human HSP60. Out of the primarily HSP-specific T cell lines, 17/23 in patients and 8/8 in controls did recognize a peptide of human origin. T cell lines specifically reactive to 136-150, 179-197, 244-258 and 336-351 could be raised with similar frequency in both groups. In contrast to a previous report, T cells also reacted to peptide 425-441 frequently in both groups. The results demonstrate that the human proliferative response to mycobacterial HSP may also target the self-protein in both BD patients and controls. However, the responsive T cells may have different effects depending on their functional features such as cytokine secretions.

Anti-alpha B-crystallin immunoreactivity in inflammatory nervous system diseases.

alpha B-Crystallin, a small heat shock protein, is an immunodominant antigen with increased tissue expression in demyelination. To investigate the humoral response against alpha B-crystallin, the sera and CSF samples of patients with multiple sclerosis (MS), Guillain-Barré syndrome (GBS), neuro-Behçet's disease (NBD) and other non-inflammatory neurological diseases (NIND) were screened by enzyme-linked immunosorbent assay for anti-alpha B-crystallin IgG and IgM antibodies. Serum and CSF IgG antibody responses to alpha B-crystallin were significantly elevated only in NBD patients (serum IgG, NBD 1.29 +/- 0.49 vs. NIND 0.95 +/- 0.39, P = 0.01; CSF IgG, NBD 1.22 +/- 0.64 vs. NIND 0.81 +/- 0.35, P = 0.01). Similarly, high serum IgM antibody titres were also detected in NBD (1.83 +/- 0.72 vs. 1.16 +/- 0.49, P = 0.0005) and in MS (1.57 +/- 1.07, P = 0.046), whereas elevated CSF IgM responses were observed only in GBS (2.09 +/- 1.09 vs. 1.41 +/- 0.7, P = 0.007). Humoral responses against alpha B-crystallin are increased in NBD and GBS, which may implicate this central nervous system antigen in the causation and pathogenesis of these inflammatory nervous system disorders.