{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,11]],"date-time":"2026-05-11T15:17:07Z","timestamp":1778512627955,"version":"3.51.4"},"reference-count":29,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,11,19]],"date-time":"2021-11-19T00:00:00Z","timestamp":1637280000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Transfusion"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Both M and N alleles encode antigens on Glycophorin A (GPA), a red blood cell (RBC) surface sialoglycoprotein. Interaction between RBC GPA and leukocyte surface lectins may downregulate their activation. The current study investigates if RBC autoantibodies against GPA, such as auto\u2010anti\u2010M\/N, prime an activated phenotype in peripheral blood leukocytes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Leukocyte activation was assessed in whole blood from patients with auto\u2010anti\u2010GPA (anti\u2010M\/N) and compared to those with allo\u2010anti\u2010M\/N and healthy subjects. Control samples from healthy subjects with no antibodies incubated in vitro with either anti\u2010GPA or anti\u2010Rh were analyzed for neutrophil and monocyte surface activation marker expression, reactive oxygen species (ROS) content, and formation of aggregates with RBCs. Samples incubated with an IgG<jats:sub>1<\/jats:sub> isotype antibody served as controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Ex vivo, neutrophil CD66b and monocyte CD63 surface expression was increased in patients with auto\u2010anti\u2010M\/N compared to those with allo anti\u2010M\/N (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.1757; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.0698) and to healthy subjects (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.0186; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.013). In vitro, neutrophil CD66b and monocyte CD63 surface expression was increased following incubation with anti\u2010GPA compared to anti\u2010Rh (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.0003; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.0328) and isotype control (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.000; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.0062). Intracellular ROS content increased in both neutrophils and monocytes incubated with anti\u2010GPA compared to anti\u2010Rh (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.0012; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.0693) and isotype control (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.001; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.0021). Percentage of neutrophil\u2010RBC aggregates was decreased when incubated with anti\u2010GPA compared to isotype control (<jats:italic>p<\/jats:italic>\u2009&lt;\u2009.01).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Neutrophils and monocytes in peripheral blood exposed to an antibody directed against GPA on RBC surfaces, such as M or N antigens, may be primed towards an activated phenotype.<\/jats:p><\/jats:sec>","DOI":"10.1111\/trf.16746","type":"journal-article","created":{"date-parts":[[2021,11,19]],"date-time":"2021-11-19T13:18:57Z","timestamp":1637327937000},"page":"217-226","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Autoantibodies to red blood cell surface Glycophorin A impact the activation poise of circulating leukocytes"],"prefix":"10.1111","volume":"62","author":[{"given":"Matthew N.","family":"Klein","sequence":"first","affiliation":[{"name":"Department of Pathology University of Maryland School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emily J.","family":"Larkin","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Maryland School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juliana N.","family":"Marshall","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Maryland School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaoxuan","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology University of Maryland School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philippe","family":"Parry","sequence":"additional","affiliation":[{"name":"University of Maryland Medical Center  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rabindra","family":"Tirouvanziam","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Emory University School of Medicine  Atlanta Georgia USA"},{"name":"Center for CF and Airways Disease Research, Children's Healthcare of Atlanta  Atlanta Georgia USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6731-9516","authenticated-orcid":false,"given":"Magali J.","family":"Fontaine","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Maryland School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2021,11,19]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2016-11-751636"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/trf.14275"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1313.006"},{"key":"e_1_2_7_5_1","volume-title":"Blood groups and red cell antigens","author":"Dean L","year":"2005"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmed.2008.06.002"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)73972-6"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M002788200"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1021\/acs.jproteome.7b00025"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.0954-6820.1982.tb03182.x"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cll.2007.05.001"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/cyto.a.22587"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1002\/9783527634286.ch12"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2017.00034"},{"key":"e_1_2_7_15_1","doi-asserted-by":"crossref","unstructured":"AbuafN RostaneH BarbaraJ Toly\u2010NdourC GaouarH Mathelier\u2010FusadeP et al.Comparison of CD63 upregulation induced by NSAIDs on basophils and monocytes in patients with NSAID hypersensitivity [monograph on the internet]. 2011. 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