The xid mutation plays an important role in delayed development of murine acquired immunodeficiency syndrome |
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Authors: | Numata F; Hitoshi Y; Uehara S; Takatsu K |
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Institution: | Department of Immunology, University of Tokyo, Japan. |
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Abstract: | Infection of C57BL/6 mice with LP-BM5 murine leukemia virus (MuLV) leads to
the development of murine acquired immunodeficiency syndrome (MAIDS)
characterized by abnormal lymphoproliferation, hypergammaglobulinemia and
severe immunodeficiency. Progression of MAIDS is delayed in X
chromosome-linked immunodeficient (XID) mice, which have an abnormality of
Bruton's tyrosine kinase (Btk) and lack functionally mature B cells
including CD5+ B cells. In this study, we report the following four major
findings. (i) Susceptibility to disease induction is not reconstituted by
transfer of CD5+ B cells to XID mice. (ii) Spleen cells from asymptomatic
XID mice are able to transmit MAIDS to wild-type mice. (iii) MAIDS can be
transmitted to XID mice with the transfer of B cells, but not T cells, from
C57BL/6 mice with MAIDS. (iv) Cells which undergo massive
lymphoproliferation in XID mice with MAIDS by cell transfer are of host
origin, but are not from the donor. We suggest from these results that a B
cell subpopulation that is impaired in XID mice plays an important role in
the initiation of MAIDS.
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