Work

B-Cell-Related Neuroinflammation Across Central Nervous System Diseases: A Bibliometric and Science-Mapping Analysis, 2006–2026

Year: 2026

Type: article

Abstract: Purpose: Research on B cells in central nervous system (CNS) diseases rests on a mature multiple sclerosis (MS) literature, whereas evidence in CNS injury and neurodegeneration is still emerging. We mapped publications from 2006 to 2026 and separated bibliometric visibility from mechanistic maturity. Methods: We searched the Web of Science Core Collection (WoSCC) on August 17, 2026, for English-language records carrying the Article document-type tag and published from January 1, 2006, through August 17, 2026. Two reviewers independently screened all records, with unresolved disagreements adjudicated by a third reviewer. Publication trends, collaboration, co-citation, journal flows, citation bursts, and keyword evolution were analyzed using VOSviewer, CiteSpace, bibliometrix, R, and SCImago Graphica. Search materials, parameters, and source tables were archived. Results: After database-level limits, 2,701 records were screened; 467 (17.3%) were excluded and 2,234 (82.7%) included. The corpus had accrued 91,218 WoSCC citations. Annual output rose from 91 articles in 2016 to 231 in 2025; 173 articles from 2026 represent a partial year. The United States contributed the most articles, and the University of California, San Francisco ranked first after affiliation normalization. Co-citation and keyword analyses showed an MS/experimental autoimmune encephalomyelitis (EAE)-centered foundation built around B-cell depletion trials, meningeal pathology, diagnostic criteria, and regulatory B-cell biology. Recent bursts included anti-CD20 therapy, single-cell RNA sequencing, autoimmune encephalitis, ischemic stroke, Mendelian randomization, B-cell depletion, and Alzheimer disease. Conclusion: B-cell-related CNS research has expanded, but evidence maturity remains disease-specific. MS/EAE provides the clearest foundation. Findings in CNS injury, neurodegeneration, and candidate peripheral-CNS routes remain context-dependent and require validation by disease, anatomical compartment, B-cell state, and stage. Bibliometric prominence reveals attention, not shared causality or therapeutic efficacy.

Source: Journal of Inflammation Research

DOI: 10.2147/jir.s635719