Submitted to: Developmental and Comparative Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/18/2004
Publication Date: 10/27/2004
Citation: Quiniou, S., Wilson, M., Bengten, E., Waldbieser, G.C., Clem, L.W., Miller, N.W. 2004. MHC RFLP analyses in channel catfish full-sibling families: identification of the role of MHC molecules in spontaneous allogeneic cytotoxic responses. Developmental and Comparative Immunology. 29(5):457-467. Interpretive Summary: Major Histocompatibility (MH) molecules play a central role in mammalian immunity but little is known about their role in fish immunity. Using DNA analyses, full sibling catfish with identical or different major histocompatibility genes sequences were identified. Assays for immunocompatibility showed that catfish MH genes were involved in the determination of self and non-self at the cellular level. As such these genes are important candidates for regulation of pathways controlling disease resistance. Variation in the MHC sequences may be useful as a tool for identification of disease resistance catfish.
Technical Abstract: Genes encoding MHC class I and II molecules have been identified in a number of fish species, including the channel catfish, but there is still a dearth of knowledge concerning their functional roles in teleost immune responses. This has in part been due to a lack of appropriate MHC class I and II matched and mismatched animals. To identify such animals, MHC segregation and linkage studies in the channel catfish were undertaken. The results of restriction fragment length polymorphism and fluorescent in situ hybridization studies showed that all the MHC class II genes are linked and most if not all MHC class I genes are linked. These studies also demonstrated that in catfish, as in other teleosts, MHC class I and II genes are not linked. Consequently, catfish matched and mismatched for MHC class I and II genes were identified and preliminary functional studies indicate that spontaneous non-specific allogeneic cytotoxic responses are likely mediated by differences in MHC class I, but not class II, region molecules.