Genetic aspects of complement and glomerulonephritis.
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Child, Preschool↗
Biomedical subjects
F Praz
Publications and source records attributed to F Praz.
Complement alternative pathway activation by chronic lymphocytic leukemia cells: its role in their hepatosplenic localization.
Using affinity-purified 125I-F(ab')2 anti-human C3, we have investigated the ability of various leukemic cells to activate complement. Lymphocytes from patients with chronic lymphocytic leukemia (CLL) activated the alternative pathway, but cells from patients with other forms of leukemia or normal lymphocytes did not do so. The amount of C3 deposited on the CLL cells was significantly higher in patients with organomegaly (i.e., splenomegaly and/or hepatomegaly). Activation of complement by CLL cells as assessed by C3 deposition on the membrane occurred both in vivo and in vitro and was not related to the N-acetylneuraminic acid content of the membrane.
Acute Disease↗
Alternative pathway of complement activation by human lymphoblastoid B and T cell lines.
Other investigators have reported activation of the alternative complement (C) pathway in homologous and heterologous serum by a variety of human lymphoblastoid B cell lines. Their ability to activate the C was associated with Epstein Barr virus transformation of the cells. We report that some human lymphoblastoid T cell lines, lacking EBV-DNA in their genome, do activate the human alternative C pathway with no participation of immunoglobulin or specific antibodies. Nevertheless, activation measured by C3 deposition on the cell surface was weaker than with the B cell lines so far studied; in relation to the RAJl cells, C3 deposition on JURKAT, MOLT 4, HSB2, and 1301 was, respectively, 68, 38, 28, and 19%. Furthermore, C3 deposition on JURKAT T cell line requires D, whereas RAJl cells provide a proteolytic activity able to mimic D, and which, unlike D, can be controlled by serum protease inhibitors. Although the ability to activate the AP seems to be a largely shared property of the human lymphoblastoid B and T cell lines, the situation was strikingly different with normal and mitogen-stimulated lymphocytes or with acute leukemic cells, which led to a negligible AP-dependent C3 deposition compared with the level observed with the lymphoblastoid cell lines. Membrane sialic acid content was determined for every cell tested and revealed no relationship with their ability to activate the AP. The two EBV+ B cell lines tested led to a comparable AP activation regardless of the presence of the C3b receptor.
Absorption↗
A one-step procedure for preparation of classical pathway (C1q) and alternative pathway (factor D) depleted human serum.
A simple method for preparation of a serum depleted in both C1q and Factor D is described. The hemolytic activities of both pathways are completely abolished and can be fully restored using the respective purified complement components. Furthermore, this serum is useful for studying cell systems since blocking either complement pathway does not require chelating agents.
Binding, Competitive↗