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Yet, its role in memory B cells (MBCs) has remained unclear. Here, we show that Fc\u03bcR\u2212\/\u2212 mice immunized with the T-dependent antigen 4-hydroxy-3-nitrophenyl acetyl-chicken \u03b3-globulin (NP-CGG) generate normal numbers of IgG1+ MBCs with long-term survival comparable to that of WT mice. However, the IgG1+ MBCs in Fc\u03bcR\u2212\/\u2212 mice contained a reduced proportion of mature CD80+PD-L2+ cells, a subset associated with potent recall responses and plasma cell differentiation. Consistently, adoptive transfer of NP-specific MBCs and CGG-specific memory T cells into Rag1\u2212\/\u2212 mice revealed significantly diminished memory B cell responses in recipients of Fc\u03bcR\u2212\/\u2212 MBCs. Mechanistically, Fc\u03bcR\u2212\/\u2212 IgG1+ MBCs exhibited impaired B cell receptor signaling and reduced activation of transcription factors essential for plasma cell differentiation upon antigen rechallenge both in vivo and in vitro. Together, these findings establish Fc\u03bcR as a previously unrecognized key regulator of CD80+PD-L2+ MBC formation and recall responses.<\/jats:p>","DOI":"10.1093\/intimm\/dxag028","type":"journal-article","created":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T07:10:20Z","timestamp":1780384220000},"page":"690-703","source":"Crossref","is-referenced-by-count":0,"title":["Fc\u03bcR enhances recall responses by promoting the generation of CD80+PD-L2+ memory B cells"],"prefix":"10.1093","volume":"38","author":[{"given":"Runyun","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences, Fudan University , Shanghai 200032 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiping","family":"Sun","sequence":"additional","affiliation":[{"name":"Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai 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