Human B-lymphocyte colony responses: Suboptimal colony responsiveness in aged humans associated with defective function of B cells and monocytes

The abilities of human B cells from young and aged subjects to form colonies in semisolid cultures stimulated with Staphylococcus protein A were investigated. Approximately three-fourths of aged adults had significantly diminished colony responses compared to young adults. In 55% of these aged adult...

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Veröffentlicht in:Cellular immunology 1985-08, Vol.94 (1), p.133-146
Hauptverfasser: Whisler, Ronald L., Newhouse, Yvonne G., Ennist, David, Lachman, Lawrence B.
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Sprache:eng
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Zusammenfassung:The abilities of human B cells from young and aged subjects to form colonies in semisolid cultures stimulated with Staphylococcus protein A were investigated. Approximately three-fourths of aged adults had significantly diminished colony responses compared to young adults. In 55% of these aged adults, the in vitro blocking of monocyte prostaglandin synthesis lead to a 1.5-fold or greater augmentation of the depressed colony responses. Other experiments showed that the improvement with indomethacin could not be explained by the greater sensitivity of aged versus young B-cell colony precursors to prostaglandin suppression. However, indomethacin failed to improve the depressed colony responses of the remaining aged adults. This failure could not be attributed to deficient interleukin 1 production, detectable alterations in accessory cell subsets of monocytes, or the lack of potential colony precursors bearing sIgD/M. Instead, the B cells from these aged subjects demonstrated a substantial decrease in the capping of sIgD/M compared to the B cells of aged subjects which displayed improved colony responses with indomethacin and compared to the B cells from young adults. Thus, these data indicate that the diminished B-cell colony responses of aged humans represent aberrancies within both the B-cell and monocyte lineages which might coexist.
ISSN:0008-8749
1090-2163
DOI:10.1016/0008-8749(85)90091-7