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Accessory and T cell defects in acquired and inherited hypogammaglobulinaemia
K E Rozynska1, G P Spickett, M Millrain
1Division of Immunological Medicine, Clinical Research Centre, Harrow, England.
Cellular defects in patients with common variable hypogammaglobulinaemia (CVH) and X-linked agammaglobulinaemia (XLA) have been studied in vitro, using a mitogen-driven system of immunoglobulin production. We have confirmed our previous finding of impaired low-density (dendritic) accessory cell function in CVH and now show that accessory cell function is normal in XLA. We demonstrate that macrophage accessory function is normal in CVH. T cell help for IgM production is also deficient in CVH, and T cell help in XLA is also abnormal for both IgG and IgM. Some XLA patients have excessive T suppressor activity. The contribution of these defects to the clinical states is discussed.
Cellular defects in patients with common variable hypogammaglobulinaemia (CVH) and X-linked agammaglobulinaemia (XLA) have been studied in vitro, using a mitogen-driven system of immunoglobulin production. We have confirmed our previous finding of impaired low-density (dendritic) accessory cell function in CVH and now show that accessory cell function is normal in XLA. We demonstrate that macrophage accessory function is normal in CVH. T cell help for IgM production is also deficient in CVH, and T cell help in XLA is also abnormal for both IgG and IgM. Some XLA patients have excessive T suppressor activity. The contribution of these defects to the clinical states is discussed.
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