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Interactions of murine leukemia virus (MuLV) with isolated lymphocytes. III. Alterations of splenic B and T cells in friend virus-infected mice

✍ Scribed by Jan Cerny; Myron Essex; D. Brian Thomas


Publisher
John Wiley and Sons
Year
1976
Tongue
French
Weight
736 KB
Volume
18
Category
Article
ISSN
0020-7136

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✦ Synopsis


Abstract

Lymphoid tissues of mice infected with murine leukemia virus (Friend) (MuLV‐F) were examined for the presence of cellular markers of MuLV‐F infection. The Friend virus‐associated cell membrane antigen (FVMA) and the virus group‐specific antigen (GSA) were detectable on cells from the spleen and, to a lesser degree, on cells from the bone‐marrow. In contrast, neither FVMA nor GSA was found in cells from the thymus. Alterations in the B‐cell and T‐cell spleen populations of MuLV‐F‐infected mice were then studied. The proportion of Ig‐positive cells declined from the initial 45% (in non‐infected controls) to about 10% after 2 weeks of infection. A similar decline of theta‐positive cells was noted. However, complement‐receptor‐bearing cells (EAC rosettes) declined even more rapidly and became undetectable in the second week after infection. The treatment of spleen cells from MuLV‐F‐infected mice with anti‐FVMA serum plus complement in vitro reduced the number of detectable Ig‐positive cells, specifically, whereas the number of theta‐positive cells remained unchanged. Furthermore, B and T cells from spleens of infected mice were separated on an affinity column with anti‐Ig antibody‐coated beads. The initial cell suspension contained about 45% FVMA‐positive cells, about 40% Ig‐positive cells and about 40% theta‐positive cells. Ig^+^ cells were retained on the column. The theta‐positive cell fraction was collected in the eluate and contained very few FVMA‐positive cells with some “null” cells. Most of the FVMA‐positive cells were retained on the column, which strongly suggested that they were B cells. These results confirm the previous experiments which showed the selective infections of purified splenic B cells by MuLV‐F in cultu.


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