Table 1 Evidence of immunological causes in patient cohorts with assumed primary forms of obsessive-compulsive disorders (extracted from [26]).

From: Immunological causes of obsessive-compulsive disorder: is it time for the concept of an “autoimmune OCD” subtype?

Pro-inflammatory cytokines

 

Gray and Bloch, 2012 (Meta-analysis) [55]

• Decreased IL-1β levels and decreased TNFα levels in non-depressed patients with OCD

• Increased IL-6 levels in adult (medication-free) patients with OCD

Jiang et al., 2018 (Meta-analysis) [56]

• TNF-α-238G/A gene polymorphism could lead to a decreased risk of OCD susceptibility

Cosco et al., 2019 (Systematic review and meta-analysis) [54]

• No alterations in different immune mediators (IL-1β, IL-4, IL-6, IL-10, TNF-α, and interferon-γ).

Antibodies/Infections

 

Pearlman et al., 2014 (Meta-analysis) [57]

• High frequency of anti-basal ganglia antibodies

Sutterland et al., 2015 (Meta-analysis) [58]

• Association with toxoplasma infection

Lamothe et al., 2018 (Systematic review) [26]

• High frequency anti-streptolysin O, anti-streptokinase, and anti-DNase B antibodies (e.g., [59])

• Anti-dopamine (D1/2) receptor antibodies and anti-lysoganglioside antibodies are more frequent in patients with PANDAS and obsessive-compulsive symptoms (e.g., [60])

• Anti-enolase antibodies are frequent [61]

• More CSF anti-brain antibody binding to basal ganglia and thalamus was described [62]

• Herpes IgG antibodies were more frequent in CSF of patients compared with controls [63]

  1. CSF cerebrospinal fluid, IgG immunoglobulin G, IL interleukin, OCD obsessive-compulsive disorder, PANDAS Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal infection, TNF tumor necrosis factor.
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