In nonpersistent disease,  a strong genetic association exists with HLA DR3-DQ2. Cardiac sarcoid has been connected to tumor necrosis factor alpha (TNFA) variants. Infectious agents
Several infectious agents appear to be significantly associated with sarcoidosis, but none of the known associations is specific enough to suggest a direct causative role. The major implicated infectious agents include: mycobacteria, fungi, borrelia, and rickettsia. A meta-analysis investigating the role of mycobacteria in sarcoidosis found it was present in 26.4% of cases, but they also detected a possible publication bias, so the results need further confirmation. Mycobacterium tuberculosis catalase-peroxidase has been identified as a possible antigen catalyst of sarcoidosis. The disease has also been reported by transmission via organ transplants. A large epidemiological study found little evidence that infectious diseases spanning years before sarcoidosis diagnosis could confer measurable risks for sarcoidosis diagnosis in the future. Autoimmune
Association of autoimmune disorders has been frequently observed. The exact mechanism of this relation is not known, but some evidence supports the hypothesis that this is a consequence of Th1 lymphokine prevalence. Tests of delayed cutaneous hypersensitivity have been used to measure progression. Pathophysiology
Granulomatous inflammation is characterized primarily by the accumulation of macrophages and activated T-lymphocytes, with increased production of key inflammatory mediators, tumor necrosis factor alpha (TNF), interferon gamma, interleukin 2 (IL-2), IL-8, IL-10, IL-12, IL-18, IL-23 and transforming growth factor beta (TGF-β), indicative of a T helper cell-mediated immune response.
Hashimotos encephalopathy, also known as steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is a neurological condition characterized by encephalopathy, thyroid autoimmunity, and good clinical response to corticosteroids. It is associated with Hashimotos thyroiditis, and was first described in 1966. It is sometimes referred to as a neuroendocrine disorder, although the conditions relationship to the endocrine system is widely disputed. It is recognized as a rare disease by the NIH Genetic and Rare Diseases Information Center.Up to 2005, almost 200 case reports of this disease were published. Between 1990 and 2000, 43 cases were published. Since that time, research has expanded and numerous cases are being reported by scientists around the world, suggesting that this rare condition is likely to have been significantly undiagnosed in the past. Over 100 scientific articles on Hashimotos encephalopathy were published between 2000 and 2013. Signs and symptoms
The onset of symptoms tends to be fairly gradual and to occur over 1-12 years.Symptoms of Hashimotos encephalopathy may include:
Personality changes
Aggression
Delusional behavior
Concentration and memory problems
Coma
Disorientation
Headaches
Jerks in the muscles (myoclonus – 65% of cases)
Lack of coordination (ataxia – 65% of cases)
Partial paralysis on the right side
Psychosis
Seizures (60% of cases)
Sleep abnormalities (55% of cases)
Speech problems (transient aphasia – 80% of cases)
Status epilepticus (20% of  cases)
Tremors (80% of cases)

Pathogenesis
The mechanism of pathogenesis is not known, but is thought to be an autoimmune disorder, similar to Hashimotos thyroiditis, as its name suggests.Consistent with this hypothesis, autoantibodies to alpha-enolase have been found to be associated with Hashimotos encephalopathy.