{"doi":"10.1096/fj.202201027","title":"The 2022 <scp>FASEB</scp> virtual Catalyst Conference on B Cells in Injury and Regeneration, March 30, 2022","abstract":"Federation of American Societies for Experimental Biology (FASEB) Catalyst Conferences are a series of half-day, virtual conferences aimed to help build communities in emerging areas of biology. Catalyst Conferences take place on Wednesdays, from October through April, and are free to attend. The second FASEB Catalyst Conference on B Cells in Injury and Regeneration took place on March 30, 2022. The meeting was co-chaired by Dr. Ruxandra F. Sîrbulescu (Principal Investigator, Vaccine and Immunotherapy Center [VIC], and Instructor in Neurology, Massachusetts General Hospital [MGH], and Harvard Medical School [HMS]) and Dr. Mark C. Poznansky (Director, Vaccine and Immunotherapy Center, MGH and Professor in Medicine at HMS, Boston, MA, USA). Together, Sîrbulescu and Poznansky assembled a panel of scientists from multiple institutions across the United States who offered a multifaceted perspective on the diverse functions that B cells can have in the context of tissue injury and regeneration. This edition of the conference focused particularly on central nervous system (CNS) injuries and on aspects of regenerative medicine. The six invited speakers shared recent published and unpublished work from their groups and others' with the stated goal of promoting open collaboration in this emerging field. Dr. Ann M. Stowe (Associate Professor, Departments of Neurology and Neuroscience, University of Kentucky College of Medicine, Lexington, KY, USA) presented recent work exploring the connection between Bcell trafficking in the brain after stroke and brain plasticity leading to improved functional outcome. Previous work from Stowe and collaborators found bilateral diapedesis of B cells into areas remote from the site of acute stroke and Bcell-mediated support for neurogenesis and functional recovery in mice.1 Interestingly, unlike other immune cells, B cells showed a lack of distinct homing to the injury site, with a widespread distribution throughout the ipsilateral and contralateral hemispheres. It is unclear, however, what parenchymal stimuli could activate B cells in remote regions ostensibly lacking canonical “pro-inflammatory” cues. Stowe proposed a mechanism by which B cells could have a trophic and neuroprotective effect after stroke through the secretion of brain-derived neurotrophic factor (BDNF). Preliminary data show that a subset of B cells responds to glutamate levels via N-methyl-D-aspartate (NMDA) receptors. In stroke, GluN2A subunit-containing NMDA receptors on B cells are activated by glutamate, leading to increased BDNF production. However, at very high glutamate concentrations, similar to levels in the epicenter of the lesion, Bcell NMDA receptor activity is reduced, potentially reducing the neuroprotective activity. Overall, Dr. Stowe hypothesizes that a subset of B cells may play a role in functional recovery after stroke by promoting neuronal survival and neuroplasticity in areas of the brain distant from the injury site through BDNF, but potential activation by physiologic levels of glutamate is concentration dependent. While there is great interest in the potential for B cells as promoters of regeneration, there are also instances where their presence at a site of injury can be detrimental. In his talk, Dr. Kristian Doyle (Associate Professor, Department of Neurology, University of Arizona, AZ, USA) described the dual nature of B cells in the context of stroke, highlighting both their neuroprotective effects and their possible role in chronic “smoldering” inflammation. Using a mouse preclinical model of ischemic stroke, Doyle described the immediate and significant increase in angiogenesis within the stroke site, characterized by the formation of new blood vessels that lack tight junctions, causing prolonged blood–brain barrier (BBB) disfunction. Moreover, due to the highly proteolytic microenvironment at the site of stroke, any newly formed tight junctions would likely be disrupted as soon as they were formed. 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Popovich","orcid":"0000-0003-1329-7395","position":3,"is_corresponding":false},{"id":632548,"name":"Elizabeth B. Engler-Chiurazzi","orcid":"0000-0002-7656-1192","position":4,"is_corresponding":false},{"id":913810,"name":"Christian LeGuern","orcid":null,"position":5,"is_corresponding":false},{"id":68265,"name":"Marion S. Buckwalter","orcid":"0000-0003-2807-2447","position":6,"is_corresponding":false},{"id":257712,"name":"Mark C. Poznansky","orcid":"0000-0003-1344-7103","position":7,"is_corresponding":false},{"id":968615,"name":"Ruxandra F. Sîrbulescu","orcid":"0000-0001-7905-1713","position":8,"is_corresponding":false},{"id":968614,"name":"Liam J. Dwyer","orcid":"0000-0001-5908-5959","position":0,"is_corresponding":true}],"reference_count":12,"raw_metadata":null,"created_at":"2026-07-19T00:30:11.069895Z","pmid":"35857314","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}