Sounds like macrophages are indeed part of the mechanism. I have absolutely no expertise or even familiarity, but hopefully a possible starting point: https://pubmed.ncbi.nlm.nih.gov/3903378/

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I can't say for sheep specifically, but most immune response is targeted at initial infection with the parasite.

In human helminthiasis, the main defenders are T-lymphocytes and eosinophils. They produce a ton of cytokines that are mainly focused on damaging/inhibiting eggs or young, very small parasites during initial infection. B cells and antibodies may be involved, but--once again--antibodies are not going to have substantive effects on the type of large intestinal worms you are talking about.

While I'm sure the host body has some immune tricks to tackle adult helminths, and others can hopefully chime in with them, by the time you have a chronic infection with large worms the parasite-host relationship is pretty established. Many helminths produce immunomodulating compounds which actively tell the immune system to not fight the worm, and, for the most part, the host is now a host and spontaneous recovery without some sort of medical intervention is unlikely.

Thank you, that's helpful! To clarify, usual practice with the sheep is to worm lambs a bit after they start grazing substantially, to hit the initial worm exposure, but then expect that after that they will have a good start on developing immunity and as adults will usually not need worming unless they are having some other kind of health challenge. That seems to fit your explanation, I think.

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I think it’s not that the adults are immune to worms, it’s that they have the capacity to carry a small to moderate parasite load without severe health effects, which is not the case for tiny babies. Economics of farming says treat the babies but leave the adults be.

(Also it really depends on which worms you’re talking about, because they each have different life cycles, but in some there is no way to truly eliminate them. I’m a vet tech but haven’t worked with sheep since undergrad so would need to brush up on them, but in adult dogs for example, common roundworms migrate out of the intestines and encyst themselves in a dormant state, then can be activated later by certain triggers, including pregnancy. I’ve been taught that 99% of puppies have roundworms, even if the mother had a negative fecal test. So we routinely aggressively deworm all puppies, and then treat adults on an as-needed case-by-case basis. https://www.merckmanuals.com/home/multimedia/image/life-cycle-of-the-toxocara-roundworm )

How would a T cell respond to an extra cellular parasite?

My vet does describe it as immunity, for what it's worth, and my understanding is that adults with "immunity" are expected to have relatively low parasite load, not only higher tolerance of parasite load. But certainly it only means relative immunity, not absolute immunity. Immune response that attacks eggs and freshly hatched parasites as the previous answer described (and as in the very cool video) seems to make sense.

ETA: I also have farm cats, and the cats get wormed every three months without fail for their whole lives (on advice of the same vet) so no expectation of immunity there. But I don't think it's economics of pets versus farm animals that is the reason for the difference, although avoidance of anthelmintic resistance is certainly a factor for the sheep.

As long as the understanding is relative/low load and not absolute/zero load, I think we’re 100% on the same page! :)

Here is a helpful paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4744952/

Currently on mobile so I'm going to do a really poor job of summarizing it, but essentially:

1. Mucus membranes help to keep parasites from attaching.

2. Innate immunity - Macrophages gobble up larvae. Circulating granulocytes (cells that carry toxic granules, think of them as bombers) and pro-inflammatory cytokine molecules make life generally unpleasant.

3. Adaptive Immunity - The big player is a class of antibody called IgE that is meant to be anti-parasite. Coordination between Helper T's, Killer T's l, IgA/IgE, etc. results in a cascade of events including: increased mucus production, attracting more granulocytes for carpet bombing, flagging parasitic cells for death (i.e. by Killer T's), reinvigorates macrophages to fight harder, etc.

Again this is a really rough summary, if you want to dive deeper I suggest checking out the paper and some of its sources! Hope this helps.

Thank you, that's great! Checking out the paper now.

ETA wow that is the exact perfect paper, thanks again!

Your second paragraph is also the basis for helminth therapy - that is, deliberate infection with helminths to tame a rampaging or dysfunctional immune system, as in autoimmune disease. Infection with certain helminths makes developing certain autoimmune diseases such as Crohn's or UC less likely, and in trials has shown to alleviate symptoms of already established autoimmune disease.