You state, "if a patient has humoral autoimmunity, with high titres of serum autoantibodies against known self-antigens." Such as what?

The short version: anti-dsDNA, anti-Sm, anti-Ro/SSA, anti-TPO, and anti-CCP are the concrete examples you asked for, and each maps to a different disease.

Anti-double-stranded DNA (anti-dsDNA) antibodies are the classic high-titer autoantibody in systemic lupus erythematosus. In one study of 207 SLE patients, 61.5% of those with lupus nephritis were positive for anti-dsDNA, compared to 34% of SLE patients without kidney involvement [3]. Another study found that 16 of 32 SLE patients (50%) had anti-dsDNA antibodies, and their presence tracked with disease activity [2]. Anti-Sm (Smith) and anti-U1-RNP antibodies are also specific to SLE: 5 of 32 SLE patients were positive for anti-Sm-D, and 18 of 32 were positive for anti-U1-RNP-A [2]. Anti-Ro/SSA and anti-La/SSB antibodies define Sjögren's syndrome and are also found in SLE. One study found anti-Ro/SSA 60 kD antibodies in 3 of 32 SLE patients and in 13 of 174 relatives, suggesting a genetic component [2].

Anti-thyroid peroxidase (anti-TPO) antibodies are the hallmark of Hashimoto's thyroiditis. In one case report, a patient with rapidly progressive hypothyroidism had an anti-TPO titer of 8,214 IU/mL, far above the normal cutoff of 34 IU/mL [30]. In a cohort of 130 patients with autoimmune hypothyroidism, all 130 were anti-TPO positive, with a mean titer around 470 IU/mL [28]. Anti-cyclic citrullinated peptide (anti-CCP) antibodies are highly specific for rheumatoid arthritis. In one study of 295 RA patients, 64.4% were anti-CCP positive, with 97.1% specificity against controls [43]. Another study found that 18 of 22 RA patients (81%) were anti-CCP positive, with 98% specificity [47].

These are the self-antigens that yield high-titer serum autoantibodies in humoral autoimmunity. The distinction from innate Th17 biology is that Th17-driven inflammation does not require any of these antibodies. You measure IL-17 in tissue, not autoantibodies in serum. The evidence records do not contain a study that directly compares both pathways in the same cohort, which is the gap that matters.

My call: anti-dsDNA, anti-Sm, anti-Ro/SSA, anti-TPO, and anti-CCP are the concrete examples. Confidence: high for the existence of these autoantibodies in their respective diseases; moderate for the distinction from Th17, because no study in this retrieval directly tests both pathways in the same system.