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Table 2 Summary of the findings from clinical studies regarding CXCL13–CXCR5 expression dysregulation in pain or neurological diseases

From: Chemokine CXCL13–CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases

Disease

Groups

Tissue

Results

Method

References

Amyotrophic lateral sclerosis (ALS)

Patients with ALS versus patients without ALS

Spinal cord motoneurons

CXCL13↑

Immunofluorescence

[104]

CSF

CXCL13↓

(p < 0.05)

ELISA

Rheumatoid arthritis (RA)

Patients with RA versus healthy controls

Plasma

CXCL13↑

(p < 0.0001)

ELISA

[88]

Patients with RA after 6 months of treatment versus baseline

Plasma

CXCL13↓

(p < 0.0001)

ELISA

Epilepsy

Patients with epilepsy versus nonepilepsy controls

Temporal neocortices

CXCL13↑

CXCR5↑

(p < 0.05)

qPCR

Immunohistochemistry

Western blotting

[108]

Multiple sclerosis (MS)

Patients with MS responding to 1 year teriflunomide treatment versus baseline

Serum

CXCL13↓

(p = 0.008)

Single molecule array

[110]

Patients with MS versus non-neurologic disease controls

CSF

CXCL13↑

(p < 0.0001)

ELISA

[119]

LNB

Patients with LNB versus non-LNB controls

CSF

CXCL13↑

(p < 0.05)

Bio-Plex Pro human cytokine array

[111]

Anti-N-methyl-d-aspartate receptor encephalitis (anti-NMDAR encephalitis)

Patients with anti-NMDAR encephalitis versus non-anti-NMDAR encephalitis controls

CSF

CXCL13↑

(p < 0.0005)

ELISA

[112]