Immune (dys)function in obsessive-compulsive disorder

It has been suggested that peripheral inflammation and immune-mediated neuronal dysfunction play a decisive role in the pathophysiology of obsessive-compulsive disorder (OCD). However, work addressing this hypothesis is mostly based on small samples and heterogeneous methodologies, and has led to inconsistent results. Here we conducted the largest study to date comparing an extensive panel of immune markers in the peripheral blood between adult patients with OCD and healthy controls.

One-hundred and thirty-nine patients with OCD and 131 age and sex-matched controls were assessed cross-sectionally for sociodemographic and clinical characteristics, and collection of peripheral blood. The concentration of high-sensitivity C-reactive protein (main outcome), of twelve cytokines, and the prevalence of positivity for anti-nuclear, anti-thyroid peroxidase, anti-thyroglobulin, and anti-basal ganglia antibodies (secondary outcomes), were assessed in the serum or plasma using ELISA. In a subsample of 176 participants, we further compared cytokine gene expression using RT-qPCR, between groups.

While patients had a significantly higher prevalence of self-reported general medical disorders, we consistently found similar levels of immune markers when comparing patients and controls, with only minor, non-significant, differences. In stratified analyses according to age of onset, current depressive episode, recruitment centre and medication status, the lack of group differences was consistent, except for higher IL-8 gene expression in patients with co-morbid depression, while subgroup analyses within the patient group revealed lower TGF-β concentration in patients with early-onset OCD.

Our findings support that, contrary to what has been shown in mood and psychotic disorders, in symptomatic and medicated adults with OCD there are only minor differences relative to healthy volunteers in cross-sectional assessments of peripheral immune markers, that may reflect co-morbid depression and/or early-onset of the disorder.