{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T19:14:21Z","timestamp":1790882061362,"version":"4.1.0"},"reference-count":50,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T00:00:00Z","timestamp":1778198400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003243","name":"Ministerstvo Zdravotnictv\u00ed Cesk\u00e9 Republiky","doi-asserted-by":"publisher","award":["MHCZ-DRO, FNOL 00098892"],"award-info":[{"award-number":["MHCZ-DRO, FNOL 00098892"]}],"id":[{"id":"10.13039\/501100003243","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007059","name":"Univerzita Palack\u00e9ho v Olomouci","doi-asserted-by":"publisher","award":["IGA_LF_2025_014 and IGA_LF_2026_013"],"award-info":[{"award-number":["IGA_LF_2025_014 and IGA_LF_2026_013"]}],"id":[{"id":"10.13039\/501100007059","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001823","name":"Ministerstvo \u0160kolstv\u00ed, Ml\u00e1de\u017ee a T\u011blov\u00fdchovy","doi-asserted-by":"publisher","award":["CZ.02.1.01\/0.0\/0.0\/16_025\/0007397, CZ.02.01.01\/00\/23_021\/0009224"],"award-info":[{"award-number":["CZ.02.1.01\/0.0\/0.0\/16_025\/0007397, CZ.02.01.01\/00\/23_021\/0009224"]}],"id":[{"id":"10.13039\/501100001823","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      IgA nephropathy (IgAN) is a mucosal immune-associated disease characterized by the overproduction of galactose-deficient IgA1 (Gd-IgA1) and formation of nephritogenic immune complexes. Epstein\u2013Barr virus (EBV), which preferentially infects IgA\n                      <jats:sup>+<\/jats:sup>\n                      B cells, has been implicated in IgAN pathogenesis, although its role remains unclear. Given mucosa involvement, we characterized breast milk B cells as available representatives of mucosal tissue to better understand the pathogenesis of IgAN.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed a phenotypic analysis of B cells (CD19\n                      <jats:sup>+<\/jats:sup>\n                      ), plasmablasts (CD38\n                      <jats:sup>+<\/jats:sup>\n                      ), and CD138\n                      <jats:sup>+<\/jats:sup>\n                      cells (representing migrating pre-plasma cells, CPC) in the breast milk of IgAN and healthy mothers (HC). EBV infection of cells was detected by using EBV-encoded RNA (EBER). B cell differentiation, IgA\/Gd-IgA1 expression, and homing-related markers were characterized using complementary cytometric and microscopic approaches.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Breast milk from mothers with IgAN contains a significantly higher proportion of EBER\n                      <jats:sup>+<\/jats:sup>\n                      B cells compared with HC. Moreover, the proportion of EBER\n                      <jats:sup>+<\/jats:sup>\n                      CPCs in the breast milk of IgAN mothers is significantly higher than in HC. B cells present in the breast milk of mothers with IgAN exhibit a higher expression of the mucosal homing receptor CCR9 compared to B cells from HC. IgA\n                      <jats:sup>+<\/jats:sup>\n                      B cells from healthy mothers exhibit a higher overall frequency of surface Gd-IgA1 expression and lack CD138 marker and thus could be classified as memory B cells or plasmablasts considering their class-switched phenotype. In contrast, breast milk from IgAN mothers was enriched for Gd-IgA1\n                      <jats:sup>+<\/jats:sup>\n                      CD138\n                      <jats:sup>+<\/jats:sup>\n                      CPC cells, indicating a shift toward terminally differentiated antibody-producing cells. These findings suggest disease-associated alterations in B cell differentiation and compartmentalization rather than increased mucosal Gd-IgA1 production\n                      <jats:italic>per se<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Despite the limited number of analyzed samples, we detected interesting differences in B cells in the breast milk of IgAN mothers and HC. The analysis of B cell populations in the breast milk of IgAN mothers indicates EBV-associated B cell dysregulation. The enrichment of EBV\n                      <jats:sup>+<\/jats:sup>\n                      CPC and Gd-IgA1\n                      <jats:sup>+<\/jats:sup>\n                      CPC in the breast milk of IgAN mothers agrees with a former model proposing aberrant mucosal B cell differentiation and trafficking involvement in IgAN pathogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1784598","type":"journal-article","created":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T05:50:18Z","timestamp":1778219418000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["IgA nephropathy-associated breast milk B cell alterations"],"prefix":"10.3389","volume":"17","author":[{"given":"Katerina","family":"Zachova","sequence":"first","affiliation":[{"name":"Department of Immunology, Faculty of Medicine and Dentistry, Palacky University Olomouc","place":["Olomouc, 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