Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unactivated human blood monocytes and monocytic THP-1 cells were found to respond to some leukemia cells by tumor necrosis factor (TNF) production. The TNF production by THP-1 cells in response to K562 cells was preceded by a rapid rise in [Ca2+]i, initiated within 1 h and terminated within 4 h as a refractory state took over. Neither the amount nor the duration of TNF production was enhanced by gamma-interferon. The P32/ISH cells did not induce a significant [Ca2+]i change of TNF production, while MOLT-4 cells failed to induce TNF despite their capacity to mobilize Ca2+ in THP-1 cells. The failure of P32/ISH or MOLT-4 to induce TNF was attributed primarily to a lack of stimulatory membrane molecules rather than to suppression by an inhibitory component, since liposomes carrying membrane components of K562 and MOLT-4 or P32/ISH in varying proportions elicited TNF production that precisely reflected the K562 proportion. The ability of K562 to induce TNF was selectively impaired by trypsin, whereas the ability to mobilize [Ca2+]i was more sensitive to glutaraldehyde, although once the latter activity was extinguished, the K562 cell could no longer induce TNF. These results suggest that some leukemia cells are equipped with two or more signaling membrane moieties which together stimulate monocytes for transient tumoricidal expression in the preimmune stage.
 ...
PMID:Lymphokine-independent, leukemia cell-mediated induction of tumor necrosis factor in human monocytes. 210 56

We have investigated the phenotype of cells positive for IL-4 and IL-5 mRNA in the nasal mucosa of subjects with allergic rhinitis and in bronchoalveolar lavage and bronchial biopsies from atopic asthmatic subjects. The method employed was immunochemistry followed by in situ hybridization using either 35S- or digoxigenin-labelled riboprobes. With nasal and bronchial tissue, this double ICC/ISH method revealed that more than 70% of IL-4 and IL-5 mRNA+ cells were T cells. The remaining IL-4 and IL-5 signals were co-localized to tryptase-positive mast cells and EG2+ eosinophils. Occasional IL-4 and IL-5 mRNA cells were observed in non-asthmatic control subjects, the large majority being CD3+ cells. These results indicate that CD3+ cells are the principal cellular source of IL-4 and IL-5 transcripts in atopic asthma and allergic rhinitis.
 ...
PMID:Phenotype of cells positive for interleukin-4 and interleukin-5 mRNA in allergic tissue reactions. 761 32