Treatment with etretinate in a patient with multiple keratoacanthoma is described. Clinical improvement correlated with normalization of IL-2-production and mitogen induced lymphocyte proliferation. A causal relationship between reduced IL-2-production and eruption of keratoacanthoma is suggested.
Speen cells derived from sheep red blood cell (SRBC)-primed nude mice gave a typical secondary response when challenged in vitro with SRBC in the presence of SRBC-primed T cells. The results demonstrate that B memory cells of both IgM and IgG type develop in the absence of functioning T cells. Moreover, these results indicate that O-antigen-bearing cells, reactive t o phytohemagglutinin (PHA) or concanavalin A (Con A), are not involved in the initiation of B cell triggering, but rather in the differentiation step leading t o antibody-forming cells.
Numerous growth factors are involved in the regulation of tissue repair and remodelling processes. The repair process is initiated by inflammation, a phenomenon that is regulated by components of the immune response such as cytokines, matrix elements and growth factors. These locally released growth factors or cytokines induce the recruitment, activation, mitogenesis and differentiation of various other cell types. It is improbable that all of them play a key role in the tissue repair process. Obviously, each of these factors may also influence normal tissue homeostasis. Therefore, the possible use of these factors for therapeutic intervention has to be considered carefully. Some of the important aspects of growth factors with regard to this topic will be discussed.
Tumor necrosis factor (TNF), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. A stable prostacyclin analogue (iloprost) was investigated for its ability to interfere with TNF secretion of lipopolysaccharide (LPS)-stimulated macrophages. It could be demonstrated by bioassays that LPS-induced TNF production was suppressed in a dose-dependent manner when macrophages were treated with iloprost at the time of LPS stimulation. Northern blot analysis revealed that iloprost inhibited TNF production at the transcription level. In vivo, endotoxin-induced mortality rates in galactosamine-sensitized mice could be significantly (P less than .05) reduced by iloprost administration. It is assumed that prostacyclin modulates endotoxin-induced and TNF-mediated inflammation in septic shock.
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