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Results for “Immunologic Capping”

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At least 595 records · Page 33Linked to original sources
PubMed1984

Evidence for the separate molecular expression of four distinct polymorphic Ia epitopes on cells of DR4 homozygous individuals.

The monoclonal antibodies 109d6 and IVD12 reacted with separate polymorphic Ia epitopes in immunofluorescent studies. Using a panel of lymphoblastoid B cell lines, antibody 109d6 reacted with all HLA-DR4 or DR7 positive lines in a pattern resembling the MT3 specificity recognized by human alloantisera. The antibody IVD12 reacted with all HLA-DR4 and two of three DR5 positive B cell lines suggesting that it recognized a specificity similar to MB3. The intensity of fluorescence was greater on DR5(+) cell lines than on DR4(+) cell lines relative to the amount of a nonpolymorphic Ia determinant. Among 45 unrelated control individuals reactivity with antibody 109d6 was correlated most closely with (r = 0.724) but not identical in occurrence to the MT3 specificity. Cocapping experiments demonstrated that the 109d6 epitope and the IVD12 epitope were present on independently redistributed cell surface molecules of DR4 homozygous lymphoblastoid cell lines. Furthermore, the DR4 alloantigens detected by an absorbed polyclonal human alloserum were similarly identified on molecules that were independent from those bearing either the 109d6 epitope or the IVD12 epitope. Taken together, these data indicate the existence of at least four distinct, serologically defined Ia molecular species.

Animals↗
PubMedDate not supplied

The immunoregulatory role of cholesterol and other lipids: a hypothesis.

Membrane lipids play an important role in cellular responses to exogenous signals. In immunocompetent lymphocytes, marked changes in the concentrations of membrane lipids occur following cell-antigen interaction. These changes lead to an increase in membrane fluidity, thus facilitating the microaggregation of receptor-antigen complexes. This event constitutes the inductive signal for lymphocytes. Lipid profile alterations leading to increased concentration of membrane cholesterol, of polyunsaturated lipids, or of both, bring about a decrease in membrane fluidity. The latter interferes with receptor displacement preventing delivery of an inductive signal to the responding cell. Interference with microaggregation is readily brought about in interactions involving low affinity antigens, such as tumoral antigens. We postulate that in hyperlipidemic and hypercholesterolemic states there is decreased immune responsiveness to weak antigens due to the aformentioned lipid profile alterations in the membranes of immunocompetent cells. The manner in which an increase in the concentration of the lipids mentioned can lead to decreased immune responsiveness and hence to an increased incidence of malignancies in hyperlipidemic and hypercholesterolemic states is the hypothesis presented in this paper.

Animals↗
PubMed1979

Regulation of the immune response by polyamines.

Regulation of the immune system is accomplished, in part, by numerous soluble factors and small molecules. One such class of regulatory substances may be the polyamines which are present in a variety of tissues. Stimulation of the immune response often occurs by crosslinking of lymphocyte surface proteins, followed by the production of some transmembrane signal. The activation pathway may be interrupted if certain necessary steps are blocked. It is proposed that polyamines exert regulatory influences by modulating crosslink formation; a step catalyzed by the enzyme transglutaminase. A model is outlined which describes the events initiating lymphocyte activation and the role of polyamines in this process. Certain drugs which might mimic the actions of polyamines are also discussed. During evolution of the control of growth processes in cells, relatively simple molecules (the polyamines) may have assumed a pivotal role in initiating and terminating the proliferative response. This idea has been applied to regulation of the immune system.

Animals↗
PubMed1994

Both high and low avidity antibodies to the T cell receptor can have agonist or antagonist activity.

Anti-TCR antibodies can activate or block the activation of T cells. In the present experiments, we have shown that different monoclonal antibodies to the same TCR can have either agonist or antagonist activity, and we have examined the relationship between these functional effects and the avidity of the antibody for the TCR. We show here that it is not the avidity of an anti-TCR antibody that determines whether it acts as an agonist or an antagonist. Moreover, we show that monovalent Fab fragments of agonist antibodies produce detectable changes in T cell behavior. These data suggest that T cell activation may involve not just aggregation of the TCR but also some induced change in individual ligated receptors, and that agonists may produce this change while antagonists do not. We argue that similar effects may apply to peptide-MHC ligands as well.

Amino Acid Sequence↗
PubMed2006

Myeloid precursors and acute myeloid leukemia cells express multiple CD33-related Siglecs.

OBJECTIVES: CD33 is a cell surface marker of committed myelomonocytic precursors and circulating monocytes, and is also found on acute myeloid leukemia (AML) cells. CD33 belongs to a family of sialic acid-binding cell surface proteins named Siglecs, among which there are 7 other functional CD33-related Siglecs (CD33rSiglecs). We sought to characterize the spectrum of expression of the other CD33rSiglecs on bone marrow precursors and AML cells and asked if they can potentially serve as targets for therapy. METHODS: Cell surface CD33rSiglecs were analyzed by flow cytometry. The ability of certain anti-Siglec antibodies to target toxin-mediated cell killing of Siglec-expressing cell lines was characterized and compared. RESULTS: We demonstrate that Siglecs-3, -5, -6, -7, and -9 are expressed on subsets of normal bone marrow precursors, including promonocytes and myelocytes. Furthermore, most AML (but not ALL) cells express these Siglecs. There is substantial variability in Siglec type and expression level between cases, with each having a unique "CD33rSiglec fingerprint." Individual anti-Siglec antibodies along with a saporin toxin-conjugated secondary antibody can target myelomonocytic leukemia cells for death, and targeting of multiple Siglecs improves cell killing. Cytotoxicity was further enhanced by sialidase treatment of target cells, which improves antibody binding. We also confirmed that antibody binding induced rapid internalization of Siglecs from the cell surface, which is a requirement for cell killing via saporin. CONCLUSIONS: Multiple CD33rSiglecs are expressed on normal and malignant myelomonoyctic cells. Targeting these Siglecs, possibly in combinations, could improve anti-CD33 antibody therapy or be used as an alternative to anti-CD33.

Antibodies, Monoclonal↗
PubMed2005

Type II phosphatidylinositol 4-kinase beta associates with TCR-CD3 zeta chain in Jurkat cells.

Phosphatidylinositol lipid signaling cascades are integral part of TCR-CD3 signaling. The mechanisms by which phosphatidylinositol kinases are coupled to TCR-CD3 complex remain elusive. Here we report an association of type II PtdIns 4-kinase with TCR-CD3 zeta chain upon cross-linking. Mapping studies have revealed that the C-terminal ITAM is critical for docking of the enzyme on the zeta chain. The association is shown to be tyrosyl phosphorylation dependent as mutation of Y-151 and Y-142 on the C-terminal ITAM disrupts interaction of the two proteins. Identification of the associated type II PtdIns 4-kinase revealed that the beta isoform of the enzyme interacts with the zeta chain in vivo.

1-Phosphatidylinositol 4-Kinase↗
PubMed2005

A dynamic view of the immunological synapse.

T cell activation requires interactions of T cell antigen receptors (TCR) and peptides presented by major histocompatibility complex molecules (MHCp) in an adhesive junction between the T cell and antigen-presenting cell. Stable junctions with bull's eye supramolecular activation clusters (SMACs) have been defined as immunological synapses (IS). These structures maintain T cell-APC interaction and allow directed secretion. T cells can also be activated by asymmetric hemi-synapses (HS) that allow migration during signal integration. IS and HS operate in different stages of T cell priming. Optimal effector functions may also depend upon cyclical use of IS and HS.

Animals↗