AMBOSS: https://next.amboss.com/us/article/1g0282?guid=B%2521%255D48ya%2525%2524g&aid=c911976e-7577-4000-9e68-d6f38cab1dfe&uid=2M0UTLgba#Zb0ec5efb2b5b779dfe98c146f4d4b593
Pathophysiology
"Cellular (especially T cells) and humoral immune responses are activated → active B lymphocytes produce thyroid peroxidase antibodies (TPOAbs) and thyroglobulin antibodies (TgAbs) → destruction of thyroid tissue"
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"Caused by either the expression of thyroid cell HLA antigen or molecular mimicry (thyroid proteins may be an immunological target as a response to antigens from viral or bacterial pathogens)"
AMBOSS Anki Addon highlight feature states "The most common type of autoimmune thyroiditis and the leading cause of hypothyroidism in iodine-sufficient areas. Caused by autoantibody-mediated destruction of thyroid tissue, which usually leads to hypothyroidism. Diagnosis is confirmed by positive thyroid antibodies."
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So from my understanding Hashimoto thyroiditis autoimmune pathophysiology is not fully understood. It's believed to be either Type IV HSR and/or Type II HSR with CD8+ T Cells and autoantibodies. I believe leading theory is T cell mediated damage begins first and once follicular cell damage occurs then the auto antibodies are able to target follicular cell/colloid contents like TPO and thyroglobulin.
Graves disease can present with the same antibodies, but they do not cause hypothyroidism symptoms. This is because TPO and thyroglobulin are inside the follicular cells and unable to be targeted by the antibodies.
It appears that AMBOSS stepwise order supports this from the first quote above.
Not sure the best thing to replace that sentence with, but I summarized the image in additional resources Fig 20.8