Abstract |
LP-BM5, a retroviral isolate, induces a disease featuring an acquired immunodeficiency syndrome termed murine AIDS ( MAIDS). Many of the features of the LP-BM5-initiated disease are shared with HIV/ AIDS. Our lab has shown that the interaction of B and CD4 T cells that is central to MAIDS pathogenesis requires ligation of CD40 on B cells by CD154 on CD4 T cells. Despite this strict requirement for CD154 expression, whether CD4 T cell receptor (TCR) occupancy is essential for the induction of MAIDS is unknown. To block TCR engagement, Tg mouse strains with monoclonal TCR of irrelevant peptide/MHC specificities, all on MAIDS-susceptible genetic backgrounds, were tested: the study of a panel of TCR Tg CD4 T cells controlled for the possibility of serendipitous crossreactive recognition of virus-associated or induced-self peptide, or superantigen, MHC complexes by a given TCR. The results argue that TCR engagement is not necessary for the induction of MAIDS.
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Authors | Wen Li, William R Green |
Journal | Virology
(Virology)
Vol. 360
Issue 1
Pg. 58-71
(Mar 30 2007)
ISSN: 0042-6822 [Print] United States |
PMID | 17113120
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
- Homeodomain Proteins
- Receptors, Antigen, T-Cell, alpha-beta
- Receptors, HIV
- RAG-1 protein
- CD40 Ligand
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Topics |
- Animals
- CD4-Positive T-Lymphocytes
(metabolism)
- CD40 Ligand
(metabolism)
- Gene Deletion
- Homeodomain Proteins
(genetics)
- Mice
- Mice, Inbred C57BL
- Mice, Nude
- Mice, Transgenic
- Murine Acquired Immunodeficiency Syndrome
(immunology)
- Receptors, Antigen, T-Cell, alpha-beta
(deficiency, genetics)
- Receptors, HIV
- Retroviridae
(pathogenicity)
- Virulence
(immunology)
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