Not at all, they’re not losing the defense receptors. They are “losing function” in negative regulators (genes that inhibit the function of other genes).
That means there’s a gene A that is shutting off another gene B by blocking activation of the other gene B, and this gene A is inactivated by a “loss of function” mutation in A.
So the gene A (the one that shuts off B) loses the ability to shut off gene B, but this results in activation of B, so now the function of B is turned on, leading to increased pathogen resistance.
The two next words after what you have bolded are crucial to understanding what is happening at the molecular level, and how this leads to a beneficial effect at the phenotypic level. So those really would be beneficial mutations. No, they don’t have to be information-increasing or complexity-increasing mutations at the same time, to really be beneficial mutations.