Several studies report the existence of autoantibodies in patients with OCD. Although only a few case reports and cross-sectional studies have been reported, they suggest that the presence of autoantibodies is a possible indicator for an autoimmune origin of the disorder. Based on experience with PANDAS and AP, the literature and expert opinion, preliminary “red flag signs” for potential autoimmune OCD are proposed (see Box).

Autoimmunity in antibody OCD and related conditions may be triggered by secondarily infection or exposure to non-self antigens. The underlying mechanism appears to be a transient brain viral infection early in life that creates long-lived permissive environment for autoimmunity by recruiting and activating memory T cells with immunologically tolerant properties. Moreover, recent studies show that the brain-specific T cell receptor CCL5 can be highly specific for self-antigens and induces a neuroinflammation response.

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The inflammatory immune response can lead to a variety of behavioral and cognitive symptoms, such as anxiety, depression, psychosis, addiction and OCD. The underlying neurobiological mechanisms are likely complex and involve the interaction of multiple factors, including microbiota and host genetics, as well as the innate and adaptive immune responses.

In one study, researchers found that people with OCD had significantly higher levels of the gene encoding for the protein Imoodulin in their T-cells – a key component of autoreactive cells. They also found that the expression of this protein was around six times higher in people with OCD than in healthy controls. When Imoodulin was blocked by an antibody in mice, they showed less anxiety. The researchers believe that the protein is involved in the formation of OCD symptoms by increasing a person’s vulnerability to triggering and maintaining anxiety.