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Oeztuerk, M.; Henes, A.; Schroeter, C.B.; Nelke, C.; Quint, P.; Theissen, L.; Meuth, S.G.; Ruck, T. Current Biomarker Strategies in Autoimmune Neuromuscular Diseases. Encyclopedia. Available online: https://encyclopedia.pub/entry/50650 (accessed on 01 August 2024).
Oeztuerk M, Henes A, Schroeter CB, Nelke C, Quint P, Theissen L, et al. Current Biomarker Strategies in Autoimmune Neuromuscular Diseases. Encyclopedia. Available at: https://encyclopedia.pub/entry/50650. Accessed August 01, 2024.
Oeztuerk, Menekse, Antonia Henes, Christina B. Schroeter, Christopher Nelke, Paula Quint, Lukas Theissen, Sven G. Meuth, Tobias Ruck. "Current Biomarker Strategies in Autoimmune Neuromuscular Diseases" Encyclopedia, https://encyclopedia.pub/entry/50650 (accessed August 01, 2024).
Oeztuerk, M., Henes, A., Schroeter, C.B., Nelke, C., Quint, P., Theissen, L., Meuth, S.G., & Ruck, T. (2023, October 22). Current Biomarker Strategies in Autoimmune Neuromuscular Diseases. In Encyclopedia. https://encyclopedia.pub/entry/50650
Oeztuerk, Menekse, et al. "Current Biomarker Strategies in Autoimmune Neuromuscular Diseases." Encyclopedia. Web. 22 October, 2023.
Current Biomarker Strategies in Autoimmune Neuromuscular Diseases
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This entry is adapted from the peer-reviewed paper 10.3390/cells12202456

Inflammatory neuromuscular disorders encompass a diverse group of immune-mediated diseases with varying clinical manifestations and treatment responses. The identification of specific biomarkers has the potential to provide valuable insights into disease pathogenesis, aid in accurate diagnosis, predict disease course, and monitor treatment efficacy. 

CIDP biomarkers GBS myasthenia gravis neuromuscular diseases IIM inflammation myositis

1. Introduction: The Need for Biomarkers in Inflammatory Neuromuscular Disorders

Inflammatory neuromuscular disorders are a heterogeneous group of immune-mediated diseases with diverse underlying pathomechanisms. Epidemiology, clinical manifestations, treatment strategies, and responses vary across the spectrum of disease. Common to all is a potential severe burden of disease with conceivable long-lasting disability. Designated criteria for categorisation of affected individuals into corresponding subgroups are well-established [1]. Over the last few years, our pathophysiological understanding of autoimmune inflammatory neuromuscular disorders has steadily improved. However, essential pathogenic processes remain to be studied. In this regard, the recognition of specific biomarkers could confer additional insights while informing treatment decisions. Biomarkers are characteristic features of biological processes and are detectable and quantifiable in body fluids and tissues [2]. As valuable indicators, they serve, inter alia, diagnostic, prognostic, and therapeutic purposes in diseases.
Considering the rarity and diversity of clinical manifestation of neuromuscular disorders (NMDs), the identification of specific biomarkers for each of them is essential, particularly regarding disease course prediction and improvement of daily clinical practice. In recent years, a considerable development on this matter has emerged. However, there is still a lack of objective biomarkers suitable in NMDs.

2. On the Concept of Biomarkers

The appliance of biomarkers has become increasingly relevant over the last decade. As useful tools, they serve various aspects in disease management. Biomarkers are indicators of both physiological mechanisms and pathogenic processes or responses to various interventions and treatment regimens in general [2][3]. Particularly in diagnostic, prognostic, and predictive aspects, biomarkers can contribute as helpful tools. The detection of the disease of interest is achieved by diagnostic biomarkers. The presence or alteration of a predictive biomarker forecasts probabilities of incidents following the exposure to an intervention or environmental factor [2]. Prognostic biomarkers aid in the estimation of clinical course and severity in the observed condition. Correspondingly, monitoring biomarkers can be employed in longitudinal disease assessment, detecting the status of a condition or measuring treatment effects. Detection of biomarkers may offer insights into causative pathomechanisms. Hence, biomarkers are crucial to the development of treatment strategies including targeted therapies, assisting healthcare for affected individuals and the population.

3. Biomarkers in GBS and CIDP

3.1. Current Biomarkers in GBS and CIDP

Few recognized biomarkers of GBS and CIDP are presently integrated in diagnostics and monitoring of disease courses and treatment responses. An overview of relevant biomarkers in use is given in Table 1.
Table 1. Current biomarkers in autoimmune neuromuscular diseases.
Disease Type of
Biomarker		 Biomarker Detection Method Correlation Occurence References Limitations/Comment
GBS/CIDP Diagnostic Lipooligosaccharides (LOS) with A, B, C, E, F and H loci; Serotype and sequence type of Campylobacter jejuni PCR screening, genes from published LOS loci and sequencing
Serum and CSF		 Identification of C. jejuni-associated GBS GBS and Miller-Fisher syndrome (MFS) [4][5]  
  Diagnostic Antibodies against
Campylobacter jejuni DNA-binding protein (C-Dps)		 ELISA, Western Blot
Serum		 Detection of
anti-C-Dps-IgG indicates C. jejuni related GBS		 Campylobacter jejuni-related GBS [6] Also detected in patients with C. jejuni enteritis (rarely)
  Diagnostic Metallo-proteinases (MMPS)
(MMP-9, TIMP-1)		 ELISA
Serum		 No correlation Described in CIDP [7] Not disease-specific
  Diagnostic Antibodies to peptides from myelin proteins P0, P214–25, PMP22 and connexin 32 Antigen-specific proliferation assay, Immunoprecipitation, Western Blot
Serum		 No correlation Described in GBS and CIDP [8][9][10][11][12][13][14]  
  Diagnostic
Monitoring		 Sphingomyelin (SM) Fluorescence-based assay
CSF		 Correlation with disease activity, elevated in active CIDP. Increased in GBS and CIDP [15]  
  Diagnostic Cystatin C (cysteine protease inhibitor) ELISA
CSF		 Decrease may be linked to higher cathepsin B activity (cathepsin B levels increased in CSF) Significant decrease of cystatin c levels in GBS and CIDP patients [16][17][18][19] Decrease also observed in MS patients
  Diagnostic Protein 14-3-3 Immunoblot assay
CSF		 Early detection (12 to 48 h after disease onset) in GBS Elevated in CSF of GBS and CIDP patients [20][21] Not disease-specific
  Diagnostic IL-8 Multiplex bead immunoassays
CSF		 Aid in differentiation between CIDP and GBS, including acute-onset CIDP.
CSF IL-8 in GBS > CIDP
Optimal IL-8 cutoff → 70 pg/mL		 Should be measured initially during diagnostical process
High specificity and positive predictive value		 [22] Not disease-specific
  Predictive
Prognostic		 Autoantibodies to gangliosides
(GM1, GA1, GD1a, GD1b, GalNAc-GD1a, 9-O-Acetyl GD1b, GD3, GM1, GT1a, GT1b, GT3, GQ1b, 0-Acetyl GT3, LM-1, GD1a/GD1b, GM1/GalNac-GD1a, GM1/PA, GM1/GD1a, GM1/GT1b, LM1/GA1)
IgG and IgM		 ELISA
Serum		 Correlation with clinical phenotypes and specific symptoms of GBS e.g., ophthalmoplegia and Anti-GQ1b IgG
Anti-GM1 linked to Campylobacter jejuni, titers correlate with clinical recovery and therapy response
GM1/GalNac-GD1a linked to respiratory infection		 High prevalence in GBS of Anti-GM1 and Anti-GT1a [23][24][25][26][27][28][29]  
  Predictive
Prognostic		 Antibodies against nodal and paranodal proteins:
Neurofascin (Nfasc155 and Nfasc140/186)
Contactin-1 (CNTN1)
Contactin- associated protein-1 (Caspr1)
Caspr1/CNTN1 complex
Gliomedin		 ELISA, Immunoprecipitation, cell-based Assays
Serum		 Associated with specific clinical manifestation e.g., ataxia and tremor
Poorer response to IVIg
Anti-CNTN1 seem to benefit from corticosteroids		 Nfasc155 in 4–18% of CIDP cases [30][31][32][33][34][35][36][37][38]  
  Predictive
Prognostic		 Neurofilaments
Phosphorylated neurofilament heavy protein (pNFH)
Neurofilament light chain (Nfl)		 ELISA,
Electrochemiluminescence (ECL) based immunoassay
Serum and CSF		 Indicator for neurodegeneration
Positive correlation with clinical and electrophysiological presentation in GBS
Association with disease progression and therapy outcome in CIDP		 Elevated in both serum and CSF of GBS and CIDP patients [25][39][40][41][42][43] General indicators of axonal damage, also detectable in other patient groups with evidence of structural CNS damage
  Predictive
Prognostic		 Tau-proteins ELISA
CSF		 Correlation with clinical manifestation and poorer clinical outcome Elevated in CSF of GBS and CIDP patients [25][42][44][45] Also detectable in other patient groups with evidence of structural CNS damage e.g., Alzheimer’s Disease
  Prognostic Autoantibodies against galactocerebroside
(Gal-C)		 ELISA
Serum		 Association with sensory deficits and autonomic disruption in GBS
Association with Mycoplasma pneumoniae infection		 GBS [46][47]  
  Prognostic Neuron-specific enolase (NSE) Enzyme immunoassay methods
CSF		 Higher levels correlate with a longer duration of disease Elevated in CSF of GBS and CIDP patients [48][49][50] CSF-NSE is not GBS or CIDP specific; Elevation is also observed other conditions e.g., Creutzfeldt-Jakob disease [51]
  Prognostic
Predictive
Monitoring		 Cytokines
Interferon gamma (IFN γ), Tumor necrosis factor α (TNF α), Transforming growth factor β1 (TGF β1), IL-1β, IL-4, IL-6, IL-10, IL-12, IL-16, IL-17, IL-18, IL-22, IL-23, IL-37		 ELISA based assays (multiplexed fluorescent bead-based immunoassay
Serum and CSF		 TNF α and IFN γ are elevated in GBS and correlate with clinical severity
TGF β1 levels are decreased in the early course of GBS, downregulation correlates with clinical disability
Serum levels are positively correlated with GBS disease severity and decreased after IVIg treatment (IL-17A, IL-37)
CSF IL-17A levels were positively correlated with clinical manifestation of GBS
Upregulation of IL-4 and IL-10 are linked to recovery phase in GBS
CSF and serum levels of interleukins declined after IVIg treatment		 Cytokine elevation is described in CIDP and GBS [52][53][54][55][56][57][58][59][60][61][62][63][64][65] Not disease-specific.
  Prognostic
Monitoring		 Serum complement proteins
C3, C3a, C5a, C5b-9		 Nephelometry
Serum		 Upregulation predicts poor prognosis
High C3 correlates with complement activation with high C3a und C5a
Correlation with disease activity		 Increased in GBS and CIDP [66][67][68] Not disease-specific
  Prognostic
Monitoring		 S100B protein (calcium-binding astroglial protein) ELISA
Serum and CSF		 Elevated in CSF and serum
Association with clinical severity and poor prognosis
Decrease in stable disease course		 Elevated in GBS and CIDP [42][49][50] Expression of S100B is not restricted to neural tissue; Serum levels can be increased after e.g., bone fractures or hepatic injury [69][70]
  Prognostic
Diagnostic		 Stem cell factor (SCF)
Hepatocyte growth factor (HGF)		 Multiplex bead-based ELISA
CSF		 Increased Elevated levels in CSF
CIDP > GBS
Correlation with chronicity		 [71] Value of this examination is still uncertain
  Monitoring Chemokines
CCR2, CCL7,CCL3, CCL27, CCR1, CCR5, CXCL10, CXCR3, CXCL9, CXCL12, monocyte chemoattractant protein 1 (MCP-1)		 Multiplex bead-based ELISA
Serum and CSF		 CCR2 and MCP-1 decreased in the recovery stage Increased in GBS and CIDP [25][72][73][74] Not disease-specific
  Monitoring Intercellular adhesion molecule 1 (ICAM-1)
Vascular cell adhesion molecule 1 (VCAM-1)
Vascular Endothelial Growth Factor (VEGF)		 Multiplex bead-based ELISA
CSF		 Decrease after therapy in studies
Correlation with repair processes is currently being studied		 Increased in GBS and CIDP [71][75][76] Not disease-specific
  Monitoring MicroRNAs
has-miR4717-5p (GBS)
has-miR-642b-5p (GBS)
miR-31-5p (CIDP)		 Microarray, droplet digital PCR
Serum		 High levels of miR-31-5p correlate with longer disease duration
Potential in improving personalized patient care		 Detectable in GBS and CIDP [77][78][79][80]  
MG Diagnostic
Monitoring		 Anti-AChRs (muscle nicotinic acetylcholine receptors)
IgG subtype 1 and 3		 Radioimmunprecipitation assay (RIPA) with high specificity and sensitivity, fixed cell-based assays
Serum		 Monitoring in patients with immunosuppressive treatment
Higher levels in ocular MG are associated with conversion to generalized MG
Higher levels in late-onset MG		 85% in generalized MG, highly specific for MG [81][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96][97][98][99] Lower titers in ocular MG
Inconsistent studies regarding correlation with disease severity and treatment response
  Diagnostic
Prognostic
Predictive		 Anti-MuSK (Muscle-specific kinase)
IgG subtype 4		 Radioimmunoprecipitation assay (RIPA), ELISA,
cell-based assay (CBA)
Serum		 Correlation with disease severity
Affection of facial-bulbar muscles
Early crises and challenging treatment
Worse outcome
Association with early onset MG and better response to rituximab		 5–8% of MG
30–50% of AChR-negative MG		 [100][101][102][103][104][105][106][107][108][109][110] More often in female patients
Highest sensitivity in detection via CBA
  Diagnostic Anti-LRP4 (low-density lipoprotein receptor-related protein 4)
IgG subtype 1 and 2		 Cell-based assay (CBA)
Serum		 Stronger clinical manifestation than in seronegative MG 2% of MG; higher in non-AChR and non-MuSK cases [111][112][113][114][115][116][117] Higher prevalence in female patients
Not specific for MG (e.g., found in ALS as well)
  Diagnostic
Prognostic		 Anti-Titin ELISA, Cell-based assay (CBA)
Serum		 Thymoma-associated MG
More frequent hospitalization		 20–40% in Anti-AChR-positive MG [95][118][119][120] Screening for thymoma presence should follow positive testing
  Diagnostic
Prognostic		 Anti-Kv1.4 (voltage gated potassium channel) Cell-based assay (CBA), Radioimmunoprecipitation assay (RIPA)
Serum		 Association with myasthenic crises and thymoma
Association with bulbar manifestation, myocarditis and QT-Time prolongation (Japanese population)		 11–18% (Japanese MG population) [95][121][122] More frequent in female patients
Expensive detection
  Diagnostic Anti-Rapsyn ELISA
Serum		 No correlations 15% of MG [95][123] Not MG-specific
  Diagnostic
Prognostic		 Anti-Cortactin Western Blot, ELISA
Serum		 Mild symptoms 10–25% of MG [95][124][125][126] Not MG specific
  Diagnostic
Prognostic
Predictive		 Anti-Agrin
IgG subtype 1 and 3		 ELISA; CBA; serum Correlation with limited therapeutic response and mild to severe clinical manifestation 2–5% of MG, mainly seropositive MG [95][127][128] More frequent in male patients
  Diagnostic
Prognostic
Predictive		 Micro-RNAs
miR-150-5p
miR-21-5p
miR-30e-5p
let-7 miRNA family		 Microarray, droplet digital PCR
Serum		 Correlation with treatment response
High miR-30e-5p levels are associated with risk of generalization in ocular MG		 Studied in AchR and MuSK-positive MG [129]  
IIM Diagnostic
Predictive
Prognostic		 Anti-Mi-2 ELISA, Immunoblot
Serum		 Classical DM, associated with beneficial prognosis, mild myositis, lower risk of ILD, better treatment response especially to rituximab
Correlation with disease activity
Association with HLA-DR7		 MSA
2–45% prevalence in DM		 [130][131][132][133][134][135] Positive sera may also be found by ELISA in PM patients [136]
Prevalence can only be estimated (varying among different countries)
  Diagnostic
Predictive
Prognostic		 Anti-ARS
(aminoacyl-tRNA synthetases)
Jo-1, PL-7, PL-12, EJ, OJ, KS, ZO, YRS		 RNA-Immunoprecipitation, ELISA, Line Blots,
Serum		 Association with ASyS
Higher mortality and interstitial lung disease (ILD) incidence in non-Anti-Jo-1-ARS (+)
Higher treatment dosage required		 MSA
Anti-Jo-1 15–30% in DM/PM
Others < 5%		 [134][137][138][139][140][141] Low prevalence of non-Anti-Jo-1-ARS
RNA-Immunoprecipitation not widely available
Rates of false-positive cases higher in Line Blots [140]
  Diagnostic
Predictive
Prognostic		 Anti-NXP2 (anti-nuclear matrix protein 2) Immunoprecipitation,
Western Blot
Serum		 Association with calcinosis and severe myositis, cancer development
Correlation with disease activity		 MSA
Adult and juvenile DM
1–5%		 [134][142][143][144][145] Immunoassays have been released and are currently discussed
  Diagnostic
Predictive
Prognostic
Monitoring		 Anti-MDA-5
(Melanin differentiation-associated protein-5)/CADM140		 Immunoprecipitation, Western Blot, ELISA
Serum		 Associated with clinically amyotrophic DM (CADM), ILD, poor prognosis, sever skin manifestation
Titer levels linked to disease severity and outcome		 MSA
15–20% in IIM, mainly CADM		 [133][134][146][147] Higher prevalence in Asia
More frequent in women
  Diagnostic
Prognostic		 Anti-TIF1γ/α (transcription factor 1 γ/α) ELISA, Immunoprecipitation
Serum		 Malignancy-associated DM MSA
10–15%, higher prevalence in cancer-associated DM, rare in PM		 [134][148][149][150][151][152] Cancer association is applied to adults [151]
  Diagnostic
Predictive
Prognostic		 Anti-SAE (small ubiquitin-like modifier activating enzyme) Immunoprecipitation,
Indirect Immunofluorescence test
Serum		 Cancer association
Serum levels correlate with disease activity		 MSA
1–5% in DM		 [153][154][155]  
  Diagnostic
Prognostic		 Anti-SRP
(Anti-signal recognition particle)		 RNA Immunoprecipitation, ELISA
Serum		 Associated with a rapidly progressive disease course with severe weakness
Cancer-associated SRP-IMNM		 MSA
20–25% in IMNM		 [156][157][158] More frequent in women
Primarily in adults
  Diagnostic
Prognostic		 Anti-HMGCR (3-hydroxy-3-methylglutaryl-coenzyme A reductase) Immunoprecipitation,
ELISA
Serum		 Significant association with serum creatine kinase
Higher serum muscle enzymes than in other IIM
Correlation with disease activity
Cancer association		 MSA
6–12% in IIM		 [158][159][160][161][162][163][164][165] Cave: Statin therapy!
  Predictive
Prognostic		 Serum soluble CD163 ELISA
Serum		 Biomarker for macrophage activation
Correlation with disease severity
Association with Anti-MDA5 (+) cases		 PM/DM [166][167][168] Not IIM-specific; supporting
  Diagnostic Anti-cN1A (cytosolic 5′-nucleotidase 1A) Addressable laser bead immunoassay (ALBIA), ELISA
Serum		 No correlation with disease severity Around 50% in IBM [169][170] Moderate sensitivity, high specificity in ALBIA [171]
Not IBM-specific, found also in known autoimmune diseases e.g., SLE [172]
  Diagnostic Micro-RNAs
miR-96-5p		 RTqPCR
Serum		 No correlation described Upregulation in PM, DM and Anti-Jo1 positive cases [173]  
Immune-mediated mechanisms following antecedent infections, commonly with a subset of Campylobacter jejuni strains with ganglioside-mimicking lipooligosaccharides (LOS), result in the typical clinical phenotype of progressive ascending symmetrical paresis of the limbs with hypo- to areflexia in GBS [174]. CIDP is an autoimmune neuropathy affecting peripheral nerves. The common clinical hallmark is the symmetrical weakness of distal and proximal portions of the limbs, whereas pure motor, pure sensory, and focal subtypes are described equally. A diagnostic delay occurs frequently in CIDP [174].
Impairments of the blood-nerve barrier and the blood-cerebrospinal fluid (CSF) barrier as barriers of the PNS are concomitant with the pathophysiology underlying GBS and CIDP. Tissue of peripheral nerves, serum, and CSF compose the predominant origins of biomarkers [25]. Biomarkers can also be linked to immediate damage of the PNS. 

4. Biomarkers in MG

4.1. Current Biomarkers in MG

MG is a chronic antibody-mediated autoimmune disease leading to focal or generalized muscle fatigability including respiratory symptoms or dysarthria [175][176]. Exclusive ocular symptoms (ocular MG) are possible and often represent the first clinical manifestation. Disease exacerbations inducing myasthenic crisis and ICU admission are still frequently observed. Causative auto-Abs target different components of the neuromuscular junction (NMJ) and disrupt regular transmission [177]. The prevalence is stated to be around 150–300 per million population [178]. The age of 50 years is used to distinguish between early-onset MG (EOMG) and late-onset MG (LOMG), as two peaks of incidence have been recognized [179][180]. In most cases (85%), auto-Abs against the extracellular domain of muscle nicotinic acetylcholine receptors (AChRs) are detected [84][85][86]. Biomarkers applied in MG are primarily disease-underlying auto-Abs and antigenic structures. An overview is given in Table 1. Specifically in the case of MG, the assignment of biomarkers to the initially introduced subgroups is rather ambiguous, as many functions are simultaneously fulfilled.

5. Biomarkers in IIM

5.1. Current Biomarkers in IIM

Idiopathic inflammatory myopathies (IIM) are a rare heterogenous cluster of autoimmune-mediated diseases affecting mainly skeletal muscles. Alongside typical manifestations with muscle weakness and fatiguing, IIMs are often accompanied by specific organ manifestations, including skin and lungs, among others. IIMs can be subclassified into different groups—dermatomyositis (DM), polymyositis (PM), immune-mediated necrotizing myopathy (IMNM), antisynthetase syndrome (ASyS), inclusion body myositis (IBM), and overlap myositis (OM) [181]. Importantly, clinical presentations, treatment responses, and prognoses differ strongly throughout subgroups [182]. Several supporting biomarkers, almost all of them auto-Abs, have been identified in the past and serve understanding causative mechanisms (Table 1). Nevertheless, IIMs are still deeply underdiagnosed.
Non-specific muscle enzymes including creatine kinase (CK), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and aldolase are elevated due to muscle damage and do not necessarily correlate with clinical severity or disease activity [183]. Due to the challenges involved in accurately assigning biomarkers to specific subgroups in IIMs, the researchers have chosen to focus separately on myositis-specific Abs (MSAs) and further biomarkers of interest. The respective classifications can be found in Table 1, delineating the different categories.

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Menekse Oeztuerk
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Antonia Henes
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Christina B. Schroeter
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Christopher Nelke
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Paula Quint
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Lukas Theissen
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Sven G. Meuth
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Tobias Ruck
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