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Using NanoString nCounter technology, we analyzed the gene expression profiles of 35 Kikuchi disease lymph node specimens and compared them across the subtypes. Compared with the febrile type, aLAP exhibited higher\n                    <jats:italic>AICDA<\/jats:italic>\n                    expression, a trend observed in both germinal center positive and negative cases. The aLAP specimens also showed higher expression of B\u2010cell markers; however, CD20 immunohistochemical staining did not reveal an increased number of B cells in aLAP. We therefore hypothesize that aLAP contains a higher proportion of atypical memory B cells, characterized by elevated\n                    <jats:italic>AICDA<\/jats:italic>\n                    and B\u2010cell marker expression compared with other B\u2010cell subsets. Immunohistochemical staining demonstrated that IRTA1+ atypical memory B cells were present in 64% (23\/36) of aLAP cases, significantly higher than in FebLAP (0\/8, 0%) and the febrile type (2\/11, 18%) (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001). This finding confirms that aLAP is more likely to contain atypical memory B cells compared with the other subtypes. Pathway analysis revealed that the febrile type upregulates pathways associated with TLR2 and TLR4 signaling and neutrophil degranulation, while aLAP upregulates the TNFR2 non\u2010canonical NF\u2010\u03baB pathway. RNAscope\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization demonstrated higher\n                    <jats:italic>TLR4<\/jats:italic>\n                    expression in the febrile type compared with the aLAP type. These findings suggest that the triggering microbes for each subtype may differ, leading to distinct immune responses and clinical presentations. Overall, these results provide new insights into the immunopathogenesis of Kikuchi disease and highlight the potential role of atypical memory B cells in shaping its distinct clinical presentations. \u00a9 2026 The Pathological Society of Great Britain and Ireland.\n                  <\/jats:p>","DOI":"10.1002\/path.70068","type":"journal-article","created":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T09:41:02Z","timestamp":1777455662000},"page":"399-411","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Immunological mechanisms underlying the clinical heterogeneity of Kikuchi disease: the potential role of atypical memory B cells"],"prefix":"10.1002","volume":"269","author":[{"given":"Shan\u2010Chi","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Pathology and Graduate Institute of Pathology, College of Medicine National Taiwan University  Taipei Taiwan"},{"name":"Department of 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