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Yes, this is known as seronegative autoimmune thyroiditis, or serum-negative Hashimotos

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The mechanisms of TB-500 are still being investigated, but known actions of TB4 include: Binding as an actin-binding protein to inhibit the polymerization of globular actin (G-actin) into filamentous actin (F-actin), known as actin sequestration, which results in higher G-actin levels and increased cellular motility [23, 24] TB4s ability to increase cellular motility may help progenitor cells to reach sites of injury and initiate tissue recovery [25]