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Chapter 5 : Evolution of the Host Defense System
Author:
Austin L. Hughes1
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Affiliations:
1: Department of Biological Sciences, University of South Carolina, Columbia, SC 29208
Content Type: Monograph
Publication Year:
2002
Category: Immunology
Book DOI:
10.1128/9781555817978
Chapter DOI:
10.1128/9781555817978.ch5
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Abstract:
The specific immune system includes several unique molecules found only in vertebrates: the immunoglobulins (Ig), the T-cell receptors (TCR), and the class I and class II molecules of the major histocompatibility complex (MHC). This chapter reviews recent evidence from molecular evolutionary studies regarding (i) the origin of the vertebrate immune system and (ii) the molecular mechanisms by which families of immune system genes have been diversified. Many researchers studying innate immunity have proposed that innate immune mechanisms of vertebrates share an evolutionary ancestry with those of invertebrates. The two mechanisms most commonly invoked to explain specific immunity—wholegenome duplication by polyploidization and horizontal gene transfer. Some authors have tried to implicate polyploidization in the origin of vertebrate-specific immunity. The chapter discusses four separate lines of evidence favoring the hypothesis that MHC polymorphism is maintained by a form of balancing selection; thus, unlike the vast majority of genetic polymorphisms of which we are aware, it is not a selectively neutral polymorphism. Defensins are antimicrobial peptides found in mammals; apparently related genes are found in insects, suggesting that the presence of defensins may be one aspect of innate immunity that shows evolutionary continuity between invertebrates and vertebrates. Interestingly, natural selection favoring diversity at the amino acid level is a characteristic not only of the specific immune system but also of some innate immune system genes.
Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
Figures
Evolution of the Host Defense System
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Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
/content/10.1128/9781555817978.chap5.fig5-1
Figure 1
Phylogeny and estimated divergence times of major vertebrate clades. Divergence times are based on data of Kumar and Hedges (1998) and Wang et al. (1999) .
10.1128/9781555817978/fig5-1_thmb.gif
10.1128/9781555817978/fig5-1.gif
Figure 1
Phylogeny and estimated divergence times of major vertebrate clades. Divergence times are based on data of Kumar and Hedges (1998) and Wang et al. (1999) .
Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
/content/10.1128/9781555817978.chap5.fig5-2
Figure 2
Phylogeny of Toll-related proteins, reconstructed by the neighbor-joining method of Saitou and Nei (1987) on the basis of the proportion of amino acid difference (p). Numbers on the branches are bootstrap percentages (i.e., the percentage of 1,000 pseudosamples constructed from the data by sampling sites from the data with replacement) which support the branch ( Felsenstein, 1985 ). Only values of =50% are shown. Names of molecules with known immune system expression are underlined.
10.1128/9781555817978/fig5-2_thmb.gif
10.1128/9781555817978/fig5-2.gif
Figure 2
Phylogeny of Toll-related proteins, reconstructed by the neighbor-joining method of Saitou and Nei (1987) on the basis of the proportion of amino acid difference (p). Numbers on the branches are bootstrap percentages (i.e., the percentage of 1,000 pseudosamples constructed from the data by sampling sites from the data with replacement) which support the branch ( Felsenstein, 1985 ). Only values of =50% are shown. Names of molecules with known immune system expression are underlined.
Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
/content/10.1128/9781555817978.chap5.fig5-3
Figure 3
Neighbor-joining tree of MHC class II DQ β1 domains from Bos taurus (Bota-), Bos primigenius indicus (Bopr-), and Ovis aries (Ovar-) based on the proportion of amino acid difference (p). Numbers on the branches are as in Fig. 2 .
10.1128/9781555817978/fig5-3_thmb.gif
10.1128/9781555817978/fig5-3.gif
Figure 3
Neighbor-joining tree of MHC class II DQ β1 domains from Bos taurus (Bota-), Bos primigenius indicus (Bopr-), and Ovis aries (Ovar-) based on the proportion of amino acid difference (p). Numbers on the branches are as in Fig. 2 .
Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
/content/10.1128/9781555817978.chap5.fig5-4
Figure 4
Plots of the number of nonsynonymous substitutions per nonsynonymous site (dN) versus the number of synonymous substitutions per synonymous site (dS) ( Nei and Gojobori, 1986 ) for pairwise comparisons among alleles at the human MHC class I HLA-A, HLA-B, and HLA-C loci. Separate plots were constructed for the codons encoding PCR (A) and the remainder of exons 2 and 3 (encoding the α1 and α2 domains) (B). Only within-locus comparisons are included in this figure, but the relationships are essentially the same for between-locus comparisons (data not shown). In each case, a 45° line is drawn for reference.
10.1128/9781555817978/fig5-4_thmb.gif
10.1128/9781555817978/fig5-4.gif
Figure 4
Plots of the number of nonsynonymous substitutions per nonsynonymous site (dN) versus the number of synonymous substitutions per synonymous site (dS) ( Nei and Gojobori, 1986 ) for pairwise comparisons among alleles at the human MHC class I HLA-A, HLA-B, and HLA-C loci. Separate plots were constructed for the codons encoding PCR (A) and the remainder of exons 2 and 3 (encoding the α1 and α2 domains) (B). Only within-locus comparisons are included in this figure, but the relationships are essentially the same for between-locus comparisons (data not shown). In each case, a 45° line is drawn for reference.
Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
/content/10.1128/9781555817978.chap5.fig5-5
Figure 5
Plots of the number of nucleotide substitutions per site (d) in intron 3 versus the number of synonymous substitutions per synonymous site (dS) in exons 2 and 3 in within-locus comparisons (A) and between-locus comparisons (B) of human genes from the HLA-A, HLA-B, and HLA-C loci. In each case, a 45° line is drawn for reference.
10.1128/9781555817978/fig5-5_thmb.gif
10.1128/9781555817978/fig5-5.gif
Figure 5
Plots of the number of nucleotide substitutions per site (d) in intron 3 versus the number of synonymous substitutions per synonymous site (dS) in exons 2 and 3 in within-locus comparisons (A) and between-locus comparisons (B) of human genes from the HLA-A, HLA-B, and HLA-C loci. In each case, a 45° line is drawn for reference.
Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
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Tables
Evolution of the Host Defense System
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Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5
/content/10.1128/9781555817978.chap5.tab5-1
Table 1
Duplication times of some genes on human chromosomes 1, 6, 9, and 19 alleged to be involved in polyploidization events early in vertebrate history
10.1128/9781555817978/tab5-1_thmb.gif
10.1128/9781555817978/tab5-1.gif
Table 1
Duplication times of some genes on human chromosomes 1, 6, 9, and 19 alleged to be involved in polyploidization events early in vertebrate history
Citation:
Hughes A.
2002.
Evolution of the Host Defense System,
p 65-76.
In
Kaufmann S, Sher A, Ahmed R (ed),
Immunology of Infectious Diseases.
ASM Press, Washington, DC.
doi: 10.1128/9781555817978.ch5