Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.13.3 (
histidine kinase
)
2,405
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
HK1
.4 mAb was identified based on its ability to stimulate proliferation of cloned murine CTL. Within the lymphoid lineage, mAb
HK1
.4 bound exclusively to CTL, regardless of the expression of Lyt-2 or MHC restriction.
HK1
.4 mAb also bound to 40% of bone marrow cells and less than 5% of thymocytes from all mouse strains tested. Based on the tissue distribution of the determinant with which it reacted and the ability to cross-block binding of the anti-Ly-6 mAb H9/25, mAb
HK1
.4 appeared to react with a product of the Ly-6 locus. However, significant differences were observed between the properties of mAb
HK1
.4 and other, previously described anti-Ly-6 mAb. Cell proliferation and lymphokine release by cloned CTL were stimulated by culture with mAb
HK1
.4 alone or in the presence of non-stimulatory levels of
IL-2
. This proliferation and lymphokine release were not blocked by the addition of soluble anti-Lyt-2 or anti-IL-2R mAb. Activation induced by
HK1
.4 mAb proceeds in the absence of accessory cells, of cross-linking of the TCR, or the addition of mitogens or PMA. Stimulation of cells by anti-TCR mAb was not blocked by the addition of soluble
HK1
.4 mAb, and the stimulatory effects of
HK1
.4 and anti-TCR mAb were not additive. However,
IL-2
-driven proliferation of CTL clones was dramatically inhibited by the addition of
HK1
.4 mAb.
HK1
.4 mAb had no effect on Ag-specific or lectin-facilitated cytolysis. Taken together, these data indicate that mAb
HK1
.4 operates via an
IL-2
-independent pathway of activation that is also independent of the TCR.
...
PMID:Characterization of an anti-Ly-6 monoclonal antibody which defines and activates cytolytic T lymphocytes. 325 67