Learn More
Glucocorticoids (GCS) inhibit the transcription of multiple activation-associated cytokine genes. By Northern blot analysis now we demonstrate that antiproliferative concentrations of dexamethasone and 6 alpha-methylprednisolone block mitogen-induced IL-2 gene expression in human peripheral blood mononuclear leukocytes in a concentration-dependent fashion.(More)
The etiology of ulcerative colitis (UC) and Crohn's disease (CD) remains enigmatic. Infiltrating intestinal macrophages are capable of producing the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6). We investigated the presence of IL-6, TNF-alpha and IL-1 beta mRNA transcripts in(More)
Under an immunosuppressive therapy after renal transplantation there is an increased risk of acquiring infections with a possible lethal outcome. On the basis of 4 cases it is shown that invasive diagnostic procedures are indicated when the primary noninvasive methods and therapeutical trials are unsuccessful. Early and consequent therapy of severe(More)
The mode of action of glucocorticosteroids as immunosuppressive and antiinflammatory agents is not fully understood. Glucocorticosteroids block synthesis of interleukin 1 by interfering with the transcription of the IL-1 beta gene. Glucocorticosteroids may also induce rapid degradation of IL-1 mRNA. In the presence of antigen, IL-1 is a potent(More)
The interleukin 2-diphtheria toxin-related fusion protein (IL-2-toxin) rapidly inhibits protein synthesis in IL-2 receptor (IL-2R)-bearing phytohemagglutinin-activated T cells but transiently stimulates DNA synthesis. At 7 hr after interaction with IL-2R+ phytohemagglutinin-activated T cells, IL-2-toxin-treated cells bear augmented steady-state levels of(More)
The interleukin-2 diphtheria toxin-related fusion protein (IL-2 toxin) inhibits protein and DNA synthesis IN rIL-2 (10(-10) M) stimulated T lymphoblasts in a dose-dependent fashion. However, prior to target cell death very low concentrations of rIL-2 and IL-2 toxin synergistically stimulate [3H] thymidine incorporation despite inhibition of [14C] leucine(More)
It has been documented that interleukin-6 (IL-6) supports the proliferation of purified, anti-CD3-stimulated murine T cells. We found that stimulation of human peripheral blood mononuclear cells (PBMCs) with anti-CD3 induced a significant accumulation of IL-6 mRNA, indicating that antigen-mediated T-cell activation may involve IL-6 release from accessory(More)
Hereditary deficiency of the third component of complement, C3, is found very seldom in the human. C3 deficiency is associated with severe bacterial infections revealing the central role of C3 in complement activation via the classical or alternative pathway. We describe a new hereditary C3 deficiency in strain 2 guinea pigs. Serum from these animals had a(More)
C3a and its C-terminal hexapeptide lead to a dose dependent release of biogenic amines and nucleotides stored in platelet's granules. The release reaction can be measured by tritiated serotonin or by ATP, indicated by an ATP specific bioluminescence assay. We tested the capability of C3a to induce aggregation of washed platelets. The recently described(More)