Although recent studies have suggested that a variety of cytokines released by keratinocytes and inflammatory leukocytes could contribute to induction or persistence of the inflammatory processes in psoriasis, it remains unclear how production of these cytokines is regulated in psoriatic patients. To elucidate the biologic relevance of these cytokines to the pathogenesis of psoriasis, we investigated serum levels of interleukin 1 alpha, tumor necrosis factor alpha, and interferon gamma in 21 patients with psoriasis vulgaris, together with 21 healthy controls. The mean serum levels of interleukin 1 alpha and tumor necrosis factor alpha were not significantly different from those in controls, while those of interferon gamma were significantly elevated in the patients with psoriasis. Serum levels of interleukin 1 alpha correlated negatively with clinical disease severity expressed as psoriasis area and severity index score and with duration of psoriasis. In contrast, interferon gamma levels were related, although not significantly, to disease severity. In addition, an inverse correlation was noted between the interleukin 1 alpha levels and interferon gamma levels. These results indicate that interleukin 1 alpha and interferon gamma may be relevant to the induction and perpetuation, respectively, of the inflammatory responses in psoriasis, and that these cytokines, which have similar biologic properties, may strictly regulate one another's production in vivo.

A retrospective immunocytochemical study was performed on repeated renal biopsy specimens from 47 patients with IgA nephropathy, 23 of whom received steroid therapy after the initial biopsy. Immune cells in renal tissues were detected by the immunoperoxidase method using monoclonal antibodies against common leukocyte antigens, T cells, B cells and monocytes/macrophages.Overall, glomerular infiltration of total leukocytes and monocytes/macrophages was significantly correlated with proteinuria. Interstitial infiltration of total leukocytes, T cells and monocytes/macrophages was significantly correlated with histological injury and renal dysfunction. In the steroid-treated group (group S), urinary protein and glomerular infiltration of total leukocytes and macrophages were significantly reduced at the follow-up biopsy, while these parameters remained unchanged in the nonsteroid-treated group (group N). In group S, interstitial infiltration of almost all of the various cell types, histological renal damage and renal function remained unchanged at the follow-up biopsy, while group N showed a significant increase in the number of interstitial total leukocytes, T cells and macrophages and showed a significant progression of histological renal injury.These findings suggest that glomerular immune cells, especially monocytes/macrophages, are involved in inducing proteinuria and interstitial immune cells are involved in renal deterioration. Furthermore, steroid therapy appears to reduce urinary protein and prevent the progression of tissue injury through suppression of renal infiltration of these inflammatory cells.