Behçet's disease is a systemic inflammatory disease immunologically characterized by the infiltration of CD(4)(+)T cells and polymorphonuclear cells in the affected tissues, including the eye. Despite extensive studies, neither the etiology nor the pathogenic mechanism of Behçet's disease has been clarified. Production of cytokines by T cell clones (TCC) from the ocular fluid (18 CD(3)(+)CD(4)(+)CD8 clones and 4 CD(3)(+)CD(4)(-)CD8(+) clones) and peripheral blood mononuclear cells (PBMC) (16 CD(3)(+)CD(4)(+)CD8(-) clones) of two patients with uveitis associated with Behçet's disease was investigated to understand better the immunopathology of the disease. The level of IL-8 spontaneously produced by TCC from the ocular fluid (mean: 659 pg/ml) or PBMC (536 pg/ml) of the patients was significantly higher (p<0.005, and p<0.05, respectively) than that by TCC (18 CD(3)(+)CD(4)(+)(-)CD8(+) clones) and 4 CD(3)(+)CD(4)(-)CD8(+) clones) from PBMC of healthy donors (241 pg/ml). As for the other cytokines, IL-Iα, IL-2, IL-6, IL-10, and TNF-α were produced at low but detectable amounts by the majority of TCC from the ocular fluid of patients with Behçet's disease; IL-3, IFN-Y, and GM-CSF were produced by some of TCC at low amounts; and IL-4 was not produced by any TCC tested. IL-8 production by TCC from the ocular fluid was further up-regulated upon stimulatation with PHA, but was suppressed by FK506 and hydrocortisone, though not by diclofenac sodium. Colchicine rather increased IL-8 production by these TCC. These results suggest that T cells in both the affected tissues and PBMC play an important role in the pathogenesis of uveitis associated with Behçet's disease through IL-8 and probably the other cytokines.

SUMMARYKD is an acute febrile illness in children characterized by coronary arteritls accompanied by aneurysm and thrombotic occlusion. The etiology of KD is unknown. It has been recently reported that KD is associated with the selective expansion of V/32"^ and V/?8.1 ' T cells in peripheral blood lymphocytes (PBL), by studying the T celt receptor (TCR) repertoire of in vitro activated T cells. KD may therefore be caused by a superantigen [I -3]. To understand better the Immunopathology of KD. we investigated TCR V/32 and V/^8.1 expression on both the T cells of freshly isolated PBL and T cell clones (TCC) from patients with KD. Cytokine production by TCC was also studied. Blood samples were obtained from patients with acute (n = 20) and convalescent (n = 20) KD, agematched children with non-infectious diseases {n = 18), and healthy adults (« = 20). Among these four groups, there were no significant differences in the percentages of either V/32^ or V^%.V T cells of freshly isolated PBL. The same was true for the CD4 * or CD8^ T cell subsets. One hundred and five TCC (98 CD3^ CD4" CD8-and seven CD3' CDA' CD8^) established from the affected skin, lymph node or PBL of six patients with KD were also negative for either V02 or V/?8.1 TCR. Sixty-eight of 105 TCC (65%) produced detectable levels (>5 pg/ml) of TNF-Q (6-1016 pg/ml), in the absence of any stimuli. In contrast, only 11 (10%) of 105 TCC or 7 (7%) of 97 TCC produced detectable levels of IL-2 or IL-6, respectively, in the absence of any stimuli. Stimulation with phytohaemagglutinin (PHA) and phorbol myristate acetate (PMA) induced most TCC to produce higher amounts of TNF-Q. IL-2 and IL-6. These results suggest that CD4'^ T helper cells expressing TCR-^ other than V/32 or V/38 receptor, primarily through TNF-a production, are involved in the immunopathology of KD,

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Expression of the MAGE genes encoding tumor‐rejection antigens on HLA‐A1 and ‐Cwl601 recognized by cytotoxic T lymphocytes was investigated in esophageal carcinomas at the mRNA level by the semiquantitative reverse transcription‐polymerase chain reaction method. MAGE‐1 and ‐2 genes, but not MAGE‐3, ‐3/‐6 and ‐4a/‐4b genes, were expressed in substantial proportions of the primary esophageal carcinomas and their metastatic lymph nodes. The proportion of MAGE‐positive samples in the primary esophageal carcinomas correlated with the T factor of the TNM classification (pT1: 2 of 12 tumors, pT2: 1 of 6, pT3: 12 of 29, and pT4: 7 of 18). These results have important implications for specific immunotherapy of esophageal carcinomas using MAGE‐1 gene product.

We report a case of a 15 year old boy with polyarteritis nodosa associated with antineutrophil cytoplasmic antibody (ANCA) against proteinase 3 (PR3). After months of steroid and immunosuppressant therapy, the symptoms subsided and the polyaneurysms almost disappeared. The levels of anti‐PR3 antibody and of cytokines also decreased. The results indicate that ANCA is a good indicator of this disease activity, and may play some pathogenic role in the disease.