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A Kock

Publications and source records attributed to A Kock.

5 recordsLinked to original sources
PubMed1988

Keratinocyte-derived interleukin 3.

Interleukin 3 (IL 3) initially was described as a cytokine which is produced by murine T lymphocytes and has multicolony stimulating factor (CSF) activity, activates mast cells and induces the proliferation of hematopoietic stem cell lines. In addition to T cells murine keratinocytes also produce an IL 3-like factor which according to its biological, biochemical and antigenic properties is indistinguishable from murine T cell IL 3. Moreover, by Northern blot analysis murine keratinocytes were found to express mRNA homologous to T cell IL 3 cDNA. Similarly, human keratinocytes have been shown to release an IL 3-like cytokine which also enhances the activity of natural killer cells and stimulates the release of oxygen radicals by granulocytes. However, human IL 3 mRNA could not yet be detected in human epidermal cells or epidermoid carcinoma cell lines. These findings indicate that human keratinocyte IL 3 appears to be distinct from T cell IL 3. Nevertheless, the exact nature of this cytokine remains to be clarified by sequence analysis and gene cloning. Through the production of these cytokines with IL 3-like capacity keratinocytes may participate in the regulation of the activity of different hematopoietic cells and thereby turn on early nonspecific host defense mechanisms against transformed cells and various harmful microbial organisms.

Animals↗
PubMed1984

The effect of in vitro UV irradiation on the production of IL 1 by murine macrophages and P388D1 cells.

Ultraviolet irradiation (UV) exposure may lead to the development of multiple immunologic defects. One such defect is a dysfunction of normal antigen-presenting cell (APC) activation of T lymphocytes after whole body or in vitro UV. Although the mechanism of this interaction is not clearly defined, several possibilities have been suggested. One proposal is that UV may inhibit or abrogate the APC IL 1 signal and thus prevent normal T cell activation. To investigate this possibility further, we examined the functional consequences of UV on murine peritoneal adherent cell (PAC) activation of a cloned antigen-specific T cell hybridoma (A2.2.E10). In agreement with previous reports, we found a marked UV-induced inhibition of PAC activation of A2.2.E10 after sublethal UV. To correlate this UV-APC dysfunction with UV alterations of IL 1 production, both the IL 1-producing murine macrophage cell line P388D1 and normal murine PAC were exposed to various amounts of in vitro UV and the 24-hr post-UV IL 1 activity production of these cells was determined. The results surprisingly indicated that certain amounts of sublethal UV may actually augment the production of IL 1 activity, by using a dose range that clearly inhibits antigen presentation. This UV-induced activity was cycloheximide-sensitive, suggesting that de novo protein synthesis rather than release from cells was responsible for the increased IL 1 activity. In addition, the UV-induced IL 1 activity had a m.w. of 14K, consistent with previous reports, and demonstrated pyrogen activity when tested in the rabbit pyrogen assay. Thus UV clearly inhibits normal APC function; however, this may not be due to abrogation of IL 1 production, but rather the result of UV toxicity for other complex events involved in antigen presentation.

Animals↗