Author
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BUTLER, JOHN - UNIVERSITY OF IOWA |
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WEBER, P - UNIVERSITY OF IOWA |
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LEMKE, C - UNIVERSITY OF IOWA |
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KIMURA, KAYOKO - IOWA STATE UNIVERSITY |
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SINKORA, M - CZECH ACADEMY OF SCIENCE |
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Baker, Amy |
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Vorwald, Ann |
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Lager, Kelly |
Submitted to: Porcine Reproductive and Respiratory Syndrome International Symposium
Publication Type: Abstract Only Publication Acceptance Date: 12/1/2006 Publication Date: 12/1/2006 Citation: Butler, J.E., Weber, P., Lemke, C.D., Kimura, K., Sinkora, M., Vincent, A.L., Vorwald, A.C., Lager, K.M. 2006. The selected B cell population in PRRS has a naive phenotype, undiversified repertoire and unusually hydrophobic HCDR3 [abstract]. 2006 International PRRS Symposium. Paper No. 33. Interpretive Summary: Technical Abstract: Isolator piglets infected with PRRS virus (PRRSV) develop lymphoid hyperplasia, hypergammaglobulinemia and autoimmunity. Preliminary characterization of the expanded B cell population in these animals reveals a naive population that continues to express CD2. Spectratypic analyses (CDR3 length analysis) of B cells in PRRS animals revealed the same profile in every tissue which contrasts with the pattern in SIV-infected littermates. While the spectratype was similar for different PRRSV-infected piglets, the profile was animal-specific. The CDR3 region of the antibody heavy chain (HCDR3) is the major contributor to antibody specificity and diversity, especially in swine because of their limited combinatorial diversity. Sequence analysis of the major HCDR3 lengths in PRRS indicated a highly skewed hydropathicity profile favoring hydrophobic sequences encoded by reading frame 3 of DHA and a near absence of HCDR3s with neutral charge that normally dominate hydropathicity profiles in non-PRRS animals. We propose that B cells with hydrophobic HCDR3s in PRRSV-infected piglets are targeted for T cell-independent proliferation without repertoire diversification. The ligand responsible may co-ligate the BCR to an innate immune receptor in the manner of LPS to promote B cell proliferation without T cell help. |