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Article: Lymphokine-induced macrophage aggregation: studies on the involvement of Mg2+.

Badenoch-Jones, P

Immunopharmacology

1982  Volume 4, Issue 2, Page(s) 115–123

Abstract: The divalent cation requirements of lymphokine (LK)-induced macrophage aggregation have been ... on exogenous Mg2+ but not Ca2+. By contrast, aggregation induced ty the ionophore A23187 is dependent ... investigated using a quantitative assay. It has been shown that LK-induced aggregation is dependent ...

Abstract The divalent cation requirements of lymphokine (LK)-induced macrophage aggregation have been investigated using a quantitative assay. It has been shown that LK-induced aggregation is dependent on exogenous Mg2+ but not Ca2+. By contrast, aggregation induced ty the ionophore A23187 is dependent on exogenous Ca2+ and Mg2+. Furthermore, exogenous Mg2+, at 0.5-5.0 mmol, both mimics the aggregation effects of LK and stimulates LK-induced aggregation. Additionally, both chlorpromazine and trifluoperazine inhibited aggregation indiced by LK, A23187, and exogenous Mg2+. Similarly, prostaglandin (PG)E2 inhibited, and indomethacin (10 micro M) stimulated, aggregation induced by these three agents. These results are discussed in the context of the mode of action of macrophage aggregating factor (MAgF).
MeSH term(s) Animals ; Calcimycin/pharmacology ; Calcium/metabolism ; Calcium/pharmacology ; Cell Aggregation/drug effects ; Chlorpromazine/pharmacology ; Guinea Pigs ; In Vitro Techniques ; Indomethacin/pharmacology ; Lymphokines/pharmacology ; Macrophages/cytology ; Macrophages/metabolism ; Magnesium/metabolism ; Magnesium/pharmacology ; Prostaglandins E/pharmacology
Chemical Substances Lymphokines ; Prostaglandins E ; Calcimycin (37H9VM9WZL) ; Magnesium (I38ZP9992A) ; Calcium (SY7Q814VUP) ; Chlorpromazine (U42B7VYA4P) ; Indomethacin (XXE1CET956)
Language English
Publishing date 1982-04
Publishing country Netherlands
Document type Journal Article
ZDB-ID 424423-0
ISSN 1879-047X ; 0162-3109
ISSN (online) 1879-047X
ISSN 0162-3109
DOI 10.1016/0162-3109(82)90014-5
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