What Are Autoimmune & Neuroimmune Conditions?

Autoimmune conditions occur when the immune system mistakenly produces antibodies that target the body’s own tissues. In neuroimmune conditions, this immune-mediated process specifically affects the nervous system — disrupting nerve signaling, damaging myelin sheaths, or impairing neuromuscular junctions.

A common feature of many autoimmune conditions is the presence of pathogenic autoantibodies — antibodies that circulate in the blood plasma and directly contribute to tissue damage and disease activity.

How TPE Works for Autoimmune Conditions

Therapeutic plasma exchange physically removes plasma — along with the pathogenic antibodies, immune complexes, and inflammatory mediators it carries — and replaces it with albumin or donor plasma. This mechanical removal can rapidly reduce antibody concentrations by 60-70% with a single exchange, providing faster relief than waiting for immunosuppressive medications to take effect.

For autoimmune conditions, TPE serves several therapeutic roles:

  • Acute crisis management — rapidly reducing antibody burden during disease flares
  • Bridge therapy — providing relief while longer-term immunosuppressants take effect
  • Maintenance therapy — periodic exchanges to keep antibody levels below symptomatic thresholds
  • Treatment-resistant cases — an option when conventional immunosuppression is insufficient

Conditions with Established Evidence

Myasthenia Gravis (MG)

Myasthenia gravis involves antibodies (anti-AChR or anti-MuSK) that attack the neuromuscular junction, causing fluctuating muscle weakness, drooping eyelids, difficulty swallowing, and in severe cases, respiratory compromise.

ASFA Category I — TPE is accepted as a first-line therapy for:

  • Myasthenic crisis (severe weakness with respiratory involvement)
  • Pre-surgical optimization before thymectomy
  • Acute exacerbations unresponsive to standard therapy

TPE rapidly removes the pathogenic antibodies causing neuromuscular blockade. Most patients experience measurable improvement within 2-3 exchanges, with maximal benefit after a series of 5-6 treatments.

Lupus (Systemic Lupus Erythematosus)

SLE is a systemic autoimmune condition where antibodies target multiple organ systems, potentially affecting kidneys, joints, skin, brain, and blood vessels. Immune complexes deposit in tissues and trigger inflammatory damage.

ASFA Category II (for severe, life-threatening manifestations) — TPE may be considered for:

  • Catastrophic antiphospholipid syndrome
  • Thrombotic thrombocytopenic purpura secondary to lupus
  • Diffuse alveolar hemorrhage
  • Severe cerebral lupus

Important: ASFA classifies lupus nephritis as Category IV (evidence suggests inefficacy). TPE is not indicated for lupus nephritis specifically.

TPE removes anti-dsDNA antibodies, antiphospholipid antibodies, and circulating immune complexes that drive organ damage in severe non-renal manifestations.

Multiple Sclerosis (MS)

In MS, immune cells and antibodies attack the myelin sheath surrounding nerve fibers in the brain and spinal cord, leading to neurological symptoms that vary based on lesion location.

ASFA Category II — TPE is indicated for:

  • Acute relapses that fail to respond to high-dose corticosteroids (steroid-refractory relapses)
  • Severe demyelinating episodes with significant disability

Approximately 40-70% of patients with steroid-refractory MS relapses show improvement following TPE, particularly when started early in the relapse course.

Rheumatoid Arthritis (RA)

RA involves autoantibodies (rheumatoid factor, anti-CCP) that contribute to chronic joint inflammation, synovial damage, and systemic inflammation.

ASFA Category III — TPE may be discussed for:

  • Severe, refractory RA not responsive to multiple disease-modifying agents
  • Cases with significant extra-articular manifestations (vasculitis, interstitial lung disease)

TPE is generally reserved for severe cases after biological and conventional DMARDs have been insufficient, as it removes circulating immune complexes and inflammatory mediators contributing to joint destruction.

PANS/PANDAS

Pediatric Acute-onset Neuropsychiatric Syndrome (PANS) and its subtype PANDAS involve sudden-onset OCD, tics, anxiety, and cognitive changes believed to be triggered by an autoimmune response — often following streptococcal infection — where antibodies cross-react with basal ganglia tissue.

ASFA Category II — TPE is considered for:

  • Moderate to severe cases with documented autoimmune markers
  • Cases refractory to antibiotics and anti-inflammatory treatment
  • Significant functional impairment in daily activities

Research has shown significant symptom reduction following TPE in well-selected patients with confirmed autoimmune-mediated PANS/PANDAS, particularly when combined with ongoing immune-modulating therapy.

Next Steps

If you have an autoimmune or neuroimmune condition and want to discuss whether TPE may benefit your specific situation, request a free consultation with our board-certified physician. Bring your medical records, recent lab work, and a list of current medications to help guide the evaluation.

References

  1. Connelly-Smith L, Alquist CR, Aqui NA, Hofmann JC, Klingel R, Onwuemene OA, Patriquin CJ, Pham HP, Sanchez AP, Schneiderman J, Witt V, Zantek ND, Dunbar NM. Guidelines on the Use of Therapeutic Apheresis in Clinical Practice - Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Ninth Special Issue. J Clin Apher. 2023 Apr;38(2):77-278. doi: 10.1002/jca.22043. PMID: 37017433.
  2. Winters JL. Plasma exchange: concepts, mechanisms, and an overview of the American Society for Apheresis guidelines. Hematology Am Soc Hematol Educ Program. 2012;2012:7-12.
  3. Cortese I, et al. Evidence-based guideline update: Plasmapheresis in neurologic disorders. Neurology. 2011;76(3):294-300.
  4. Lehmann HC, et al. Plasma exchange and intravenous immunoglobulins: mechanism of action in immune-mediated neuropathies. J Neuroimmunol. 2011;231(1-2):61-69.

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