Because you make some insane erroneous point about the immune system I am supposed to give you a lollypop?
Is that why you're physiologically incapable of admitting a mistake or learning anything from an opponent? Because you perceive it as giving your enemies lollypops?
It doesn't need to anticipate anything in order to promote change. All it needs is for people with rare alleles to survive epidemics at a slightly higher rate than people with more common alleles.
That is not promoting anything. It is chance contingency. The story of evolution.
That's no more "chance contingency" than evolution as a whole is creationists' caricature of evolution as "a tornado in a junkyard". It's entirely predictable from thinking about herd immunity.
Evolution is an arms race. Diseases aren't the only ones doing the evolving.
The human immune system is evolving. That was never an issue.
But it hasn't changed much in at least 200 thousand years. Because it is a complete delicate system that is constructed with many many genes.
Most single mutations would disrupt the system to the point it would decrease the likelihood of survival. They would not be beneficial.
Wrong. You are not saying that because of anything you know about the immune system. You are simply extrapolating from what you know of other systems like the auditory system, and deducing that the immune system must be as fragile as hammer, anvil and stirrup bones.
"In addition, recent research in a variety of taxa and situations has revealed that evolution often occurs on contemporary timescales, often within decades (summarised in [32]). In some cases, the time span between the separation of populations might even be too short to leave a signal at neutral loci so that differences between populations are only detectable at genes under selection [33], such as those of the highly variable major histocompatibility complex (MHC). Contrary to neutral markers, MHC variability reflects evolutionary relevant and adaptive processes within and between populations and is very suitable to investigate a wide range of open questions in evolutionary ecology and conservation. The comparison with neutral markers allows the construction of null hypotheses concerning the diversity at selectively relevant genes and conclusions on the relevance of MHC polymorphism.
...
Genes within the MHC involved in antigen presentation constitute the most polymorphic loci known in vertebrates [52, 53]. The variability of the MHC-molecules is correlated with the diversity of the T-lymphocyte receptors which in turn determine the disease and parasite resistance of an organism and thus may influence the long-term survival probability of populations [54, 55, 56, 57]. The antigen binding sites show high levels of variation not only in the number of alleles but also in the extent of sequence variation between alleles [58]. Under neutrality theory, the rate of synonymous nucleotide substitution (ds) is predicted to be larger (ds > dn) than the rate of non-synonymous substitution (dn) because non-synonymous substitutions change the amino acid composition and are thereby likely to be deleterious [59, 60]. However, several studies demonstrate that the ABS display more non-synonymous than synonymous substitutions (dn > ds) ([61, 62], reviewed by [19]). This cannot be explained by a higher mutation rate in this specific region [58, 61, 62]. The emerging general view is that the determinant role in shaping patterns of nucleotide diversity in MHC genes is balancing selection [19, 59, 60, 63]. Balancing selection results not only in the maintenance of large numbers of alleles in populations, but also in greatly enhanced persistence of allelic diversity over extremely long time periods relative to neutral genetic variation [64], an observation termed 'trans-species evolution of polymorphism' [42]. The subsequent alteration in ABS allows binding of a diverse array of antigens [61, 62, 65]."
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Source)
DNA bases in immune system genes at positions where variation changes the encoded amino acid are
more likely to be variants than bases at positions where it doesn't. That's
the opposite of the statistics in most of the genome. In most of the genome a change that makes no difference is more common. That's because chances are a change that does make a difference will be harmful, as you say. "Most single mutations would disrupt the system". Do the math. The reason SNPs in MHC genes have the opposite statistics from normal is because
mutations in MHC genes are more likely to be beneficial than harmful.
Unless of course you think some god is controlling random mutations.
Unless of course the only reason you think it would take a god controlling random mutations in order for there to be a bias toward beneficial mutations is because, as Crick said, "Evolution is cleverer than you are".