Open AccessCD4 depletion in HIV‐infected haemophilia patients is associated with rapid clearance of immune complex‐coated CD4 + lymphocytes
Author(s) -
Volker Daniel,
Anette Melk,
Caner Süsal,
Rolf Weimer,
Rainer Zimmermann,
Angela HuthKühne,
Gerhard Opelz
Publication year - 1999
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1999.00848.x
Subject(s) - immune system , immunology , immune complex , haemophilia , viral load , biology , immunopathology , pathogenesis , lymphocyte , virus , genetics
The predominant immunological finding in HIV + haemophilia patients is a decrease of CD4 + lymphocytes during progression of the disease. Depletion of CD4 + lymphocytes is paralleled by an increase in the proportion of immune complex‐coated CD4 + cells. We examined the hypothesis that the formation of immune complexes on CD4 + lymphocytes is followed by rapid clearance of immune complex‐coated CD4 + lymphocytes from the circulation. In this study, the relationship of relative to absolute numbers of immune complex‐loaded CD4 + blood lymphocytes and their association with viral load were studied. Two measurements of relative and absolute numbers of gp120‐, IgG‐ and/or IgM‐loaded CD4 + lymphocytes were analysed in HIV + and HIV − haemophilia patients, with a median interval of approx. 3 years. Immune complexes on CD4 + lymphocytes were determined using double‐fluorescence flow cytometry and whole blood samples. Viral load was assessed using NASBA and Nuclisens kits. Whereas the proportion of immune complex‐coated CD4 + lymphocytes increased with progression of the disease, absolute numbers of immune complex‐coated CD4 + lymphocytes in the blood were consistently low. Relative increases of immune complex‐coated CD4 + blood lymphocytes were significantly associated with decreases of absolute numbers of circulating CD4 + lymphocytes. The gp120 load on CD4 + blood lymphocytes increased in parallel with the viral load in the blood. These results indicate that immune complex‐coated CD4 + lymphocytes are rapidly cleared from the circulation, suggesting that CD4 + reactive autoantibodies and immune complexes are relevant factors in the pathogenesis of AIDS. Relative increases of immune complex‐positive cells seem to be a consequence of both an increasing retroviral activity as well as a stronger loading with immune complexes of the reduced number of CD4 + cells remaining during the process of CD4 depletion. The two mechanisms seem to enhance each other and contribute to the progressive CD4 decrease during the course of the disease.