Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0393754 (HSA)
 2,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Desensitization of human basophils with anti-IgE antibody or antigen induced an increased sensitivity to the phorbol ester TPA, evidenced as 2-5 fold increase in the potency of TPA to induce histamine release. As noted in previous publications the magnitude of the change in sensitivity to TPA was a function of the extent of cell surface IgE crosslinking. Thus, the density of cell surface antigen-specific IgE determined the magnitude of the curve shift and the multivalent antigen, BPO21-HSA was found to produce a greater curve shift than the simpler bivalent hapten, BPO2, in accord with previous studies which demonstrated that BPO2 was a "weak" stimulus compared to BPO21-HSA. Basophils which had been fully desensitized by prior treatment with anti-IgE or antigen in the absence of calcium also displayed the curve shift for at least 24 h after desensitization. However, the change induced by crosslinking which altered the cells' sensitivity to TPA required the continued presence of crosslinks and was therefore not the result of a permanent alteration induced by desensitization. Basophils which were fully desensitized to BPO7-HSA demonstrated the curve shift provided that the antigen-induced crosslinks were maintained: treatment with monovalent hapten, BPO-EACA, rapidly returned the cell response to TPA to control, non-desensitized, levels. Since TPA is thought to act by activation of protein kinase C (PKC) we demonstrated that BPO-HSA induced crosslinking increased PKC activity and that the increased activity persisted unless antigen-induced crosslinks were dissociated by the addition of monovalent hapten.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistence of early crosslink-dependent signal transduction events in human basophils after desensitization. 245 86

The introduction and expression of allogeneic MHC class I genes in tumors can generate tumor-specific immunity which subsequently results in the regression of parental tumors. Immunization of naive (AKR/J x C57BL/6)F1 mice with H-2Kb-transformed K36 tumor cells was found to render recipient mice immune to a subsequent challenge by parental K36 tumor cells. Two types of cytotoxic T effector cells were demonstrated in these immune mice. One of the cytotoxic effector cells generated against the K36 tumor cells is the conventional CD3+ cells, and these account for approximately one-third of the total observed tumor-specific cytotoxicity in vitro. The other cytotoxic effector cell generated following the immunization of (AKR/J x C57BL/6)F1 mice with the H-2Kb-transformed K36 cells had the CD3-/Thy-1+ phenotype, and accounted for the remaining two-thirds of the observed tumor-specific cytotoxicity in vitro. These CD3-/Thy-1+ cells can lyse parental K36 tumor cells in a tumor-specific fashion, and tumor-specific immunity can be adoptively transferred to naive animals via the CD3-/Thy-1+ cells. In contrast to CD3+ CTL, CD3-/Thy-1+ cells express CD45RBlow, Ly-6Chigh, and HSA molecules. Although the CD3-/Thy-1+ cells can be activated in vitro by IL-2, TPA, and ionomycin, they cannot be propagated in vitro. The CD3-/Thy-1+ cells undergo apoptosis following prolonged culture in vitro. At present, the exact mechanism(s) by which CD3-/Thy-1+ cells can mediate tumor-specific cell lysis in the absence of identifiable T cell receptor molecules is unknown; nevertheless, these data suggest the existence of a novel T cell type to combat tumors.
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PMID:Characterization of tumor-specific cytotoxic effector cells with a novel CD3-/Thy-1+ phenotype. 758 74