The fishy disappearance of MHCII genes: evolution of MHCI genes leads to an alternative acquired immune response in Atlantic cod.

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Genes for major histocompatibility complex (MHC) are important for the function of the adaptive immune system [1]. MHCI molecules usually present endogenous antigens to cytotoxic T cells. However, T helper cells are activated by exogenous antigen presentation on MHCII. Post infection memory and immunity also depends on this action of MHCII. Errors in the MHCII pathway are usually associated with immune-deficiency and disease. The alternative cross regulation pathway requires MHCI molecules to copy MHCII molecules and present exogenous antigen and depends on the trafficking facilitated by adapter proteins [2, 4]. These proteins recognize and bind to conserved sorting sequences in the cytoplasmic domain acting as signals [2, 3]. Di-leucine-based and tyrosine-based signal sequences are the main signals seen for endosome trafficking. In humans both these signals are involved in MHCI cross presentation. Studies sequencing the complete genome of Atlantic cod showed important MHCII pathway components required for T cell activation were missing and an expanded repertoire of MHCI genes [5,6]. There are two conflicting ideas as to the reason behind this, some think that the loss of MHCII function caused MHCI genes to gain additional functionality and expand into two distinct groups. Malmstrom et al. link this unique MHC gene organization to the structure of the MHC by showing that MHCI molecules have novel combinations of signal sequences which possibly led to MHCII like function. Using spleen tissue they generated cDNA through the use of PCR reactions in order to complete coding region of MHCI. They then examined the binding pocket component encoded by this data and were able to identify several conserved structural and functional sequence... ... middle of paper ... ...n the past. Evolution such as this helps to battle the every changing pathogens. References 1. Malmstrom M. et al. PLoS ONE 2013, 8:9 2. Breitfeld P.P. et al. Current Opinion in Cell Biology 1989, 1: 617–623 3. Mellman I. Annu Rev Cell Dev Biol 1996, 12: 575–625. 4. Kovacsovics-Bankowski M, Rock K.L. Science 1995, 267: 243–246 5. Landsverk O.J. et al. Scand J Immunol 2009, 70: 184–193. 6. Persson A.C. et al. Immunogenetics 1999, 50: 49–59 7. Borghans J.A.M. et al. Immunogenetics 2004, 55(11): 732-739 8. Miller K.M. et al. Immunogenetics 2002, 53(10-11): 941-963 9. Trowsdale J. Immunogenetics 1995, 41(1): 1-17 10. Lawlor D.A. et al. Annu Rev Immunology 1990, 8:23-63 11. Singer D.S. and Maguire J.E. Crit Rev Immunology 1990, 10(3):235-257 12. Landsverk O.J.B. et al. Scand J Immunology 2009, 70(3):184-193 13. Persson A.C. et al. Immunogenetics 1999, 50(1-2):49-59
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