B‐Lymphocyte Alloantigens

Johnson, Anne H.; Ward, Frances E.; Amos, D. Bernard

doi:10.1111/j.1365-3083.1977.tb02095.x

Cited by 11 publications

(6 citation statements)

References 7 publications

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“…Several peptides based on these sequences were synthesized; those peptides that mimicked the sequences around the tryptophan residue at position 277 of human IgGl fixed complement (208). These results confirm the hypothesis (183) that this tryptophan moiety is part of the complement-fixing site (209). These sequences surrounding this aromatic amino acid are hydrophobic and also contain anionic side-chain amino acid residues.…”

Section: Search For Anticomplement Drugssupporting

confidence: 90%

Complement: A Host Defense Mechanism Ready for Pharmacological Manipulation?

Johnson

1977

Journal of Pharmaceutical Sciences

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Section: Search For Anticomplement Drugssupporting

confidence: 90%

Complement: A Host Defense Mechanism Ready for Pharmacological Manipulation?

Johnson

1977

Journal of Pharmaceutical Sciences

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“…An important product of this pathway is leukotriene B 4 (LTB4), which is a very potent neutrophil chemotaxin and also stimulates neutrophil degranulation and oxidative burst activity (12). LTB 4 can have pro-inflammatory effects on mononuclear cells, including enhancement of production of the key inflammatory cytokines interleukin-1 (13,14), interleukin-2 (15) and interferon-gamma (15,16). LTB 4 inhibits mitogen-induced proliferation of CD4 § T cells and enhances proliferation of CD8 § T cells (17,18) and, accordingly, may also modulate immunological responses.…”

mentioning

confidence: 99%

Inhibition of human neutrophil leukotriene B₄ synthesis in essential fatty acid deficiency: Role of leukotriene a hydrolase

Cleland

James

Proudman

et al. 1994

Lipids

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A female subject dependent on long-term total parenteral nutrition developed an aversion and noncompliance to a prescribed weekly lipid infusion designed to meet essential fatty acid (EFA) requirements. Fatty acids (FA) in the subject's plasma and isolated peripheral blood neutrophils were analyzed in search of biochemical evidence of EFA deficiency. Neutrophil 5-lipoxygenase metabolism was examined to assess the possible effects of EFA deficiency on neutrophil eicosanoid metabolism. EFA deficiency was confirmed by marked depletion of linoleic acid (18:2n-6) and accumulation of eicosatrienoic acid (ETrA; 20:3n-9) in plasma and neutrophil phospholipids. In the neutrophils, ETrA comprised 5.2% of phospholipid FA (normal reference values < 0.1%), and arachidonic acid (AA; 20:4n-6) comprised 8.6% of phospholipid FA (normal reference range 10-16%). When stimulated by A23187 in vitro on three separate occasions, the subject's neutrophils displayed impaired synthesis of leukotriene B4 (LTB4), but produced normal amounts of 5-hydroxy-eicosatetraenoic acid and all-trans isomers of LTB4 formed nonenzymatically from leukotriene A4 (LTA4). This pattern of synthesis suggested inhibition of LTA hydrolase and was also seen in neutrophils from healthy subjects by addition of exogenous ETrA in vitro. Comparative studies of the effects of ETrA and eicosapentaenoic acid (20:5n-3) on neutrophils in vitro suggested that ETrA is the more potent inhibitor. Accumulation of ETrA, rather than depletion of AA, appears principally responsible for the observed impairment of neutrophil LTB4 synthesis seen in this EFA-deficient subject.

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“…Leukoregulin is a unique lymphokine that rapidly induces nonlethal membrane permeablization in K562 cells. This form of membrane destabilization is partially dependent on extracellular Ca++ unlike the totally calcium-dependent target cell inhibitory action of many other products of cytotoxic T cells, e.g., cytolysin and perforin [7][8][9] and some lymphokines, e.g., lymphotoxin [4] and interleuhn-2 [29]. The membrane permeability changes induced by leukoregulin correlate closely with subsequent changes in cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Influence of extracellular calcium on cell permeabilization and growth regulation by the lymphokine leukoregulin

Barnett

Evans

1990

J of Cellular Biochemistry

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Permeablization of human K562 leukemia cells was measured in the presence and absence of extracellular ionic calcium to examine the relationship of ionic calcium to increased membrane permeability and the inhibition of cell proliferation by this lymphokine. In the absence of extracellular calcium, the ability of leukoregulin to permeabilize the cell membrane is diminished but is fully restored by addition of 1 mM extracellular Ca++ as shown flow cytometrically by loss of intracellular fluorescein. Membrane permeability is also increased by calcium ionophore A23187 but permeablization is completely blocked in calcium-free medium despite the intramembrane presence of the calcium ionophore. Membrane permeablization by the lectin phytohemagglutinin, in contrast, is independent of extracellular calcium. A similar divergence in cell proliferation activity of the three modulators of calcium flux and membrane permeability occurs in the absence of extracellular calcium. Leukoregulin inhibition of cell proliferation is abolished, inhibition by calcium ionophore A23817 is greatly reduced, and inhibition by phytohemagglutinin is unchanged. Leukoregulin permeabilized K562 cells isolated by fluorescence activated cell sorting resume proliferation after 72 h. In contrast cells permeablized by calcium ionophore A23187 or phytohemagglutinin fail to resume proliferation by 7 days. The membrane permeablizing action of leukoregulin is, therefore, partially dependent upon extracellular calcium. It is also effected through a mechanism other than calcium ionophore transport or lectin type transmembrane signaling, and is accompanied by a reversible inhibition of cell proliferation.

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B‐Lymphocyte Alloantigens

Cited by 11 publications

References 7 publications

Complement: A Host Defense Mechanism Ready for Pharmacological Manipulation?

Complement: A Host Defense Mechanism Ready for Pharmacological Manipulation?

Inhibition of human neutrophil leukotriene B₄ synthesis in essential fatty acid deficiency: Role of leukotriene a hydrolase

Influence of extracellular calcium on cell permeabilization and growth regulation by the lymphokine leukoregulin

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B‐Lymphocyte Alloantigens

Cited by 11 publications

References 7 publications

Complement: A Host Defense Mechanism Ready for Pharmacological Manipulation?

Complement: A Host Defense Mechanism Ready for Pharmacological Manipulation?

Inhibition of human neutrophil leukotriene B4 synthesis in essential fatty acid deficiency: Role of leukotriene a hydrolase

Influence of extracellular calcium on cell permeabilization and growth regulation by the lymphokine leukoregulin

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Inhibition of human neutrophil leukotriene B₄ synthesis in essential fatty acid deficiency: Role of leukotriene a hydrolase