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• W3211423020 abstract "Maternofetal transfusion, the transfer of maternal cells leading to chimerism in the offspring, is a complicated setup. The role of maternofetal transfusion, its consequences, maternal engraftment, and graft versus host disease (GvHD) become further known after the studies on patients with severe combined immunodeficiency (SCID). Maternofetal transfusion may lead to cellular engraftment at first in the blood, soon in the tissues of the fetus and the newborn. The engraftment of maternal cells and resultant GvHD may cause severe tissue inflammation and autoimmunity. The symptoms of the GvHD caused by maternal engraftment (ME) in patients with SCID are similar to the symptoms of GvHD caused after hematopoietic stem cell transplantation. The effect of inflammatory cells is generally on the skin, liver, and gastrointestinal tract. When a patient with SCID presents with extensive tissue inflammation except for infectious inflammation, the differential diagnosis of ME and GvHD includes another disease, Omenn syndrome, a systemic inflammatory reaction experienced again in patients with SCID. In Omenn syndrome, primary cells causing tissue inflammation are the oligoclonal expanded reactive cells, whereas tissue-infiltrating cells are of maternal origin in GvHD due to ME. The CD45RA+ (naive)/CD45RO+ (memory) cell ratio matters because the naive and memory states of the inflammatory cells differ in both diseases. Severe inflammation in ME and GvHD is related to several factors. One of these factors is the number of transferred cells. The characteristics of these chimeric cells, such as cell type (myeloid, lymphoid lineage), proliferation capacity after stimulation (immune competence), differentiation step (stem cell, progentior cell, or mature cell), diversity (TCR and BCR repertoire), HLA typing, and its compatibility between the mother and the fetus seem to be other factors. There is generally an HLA incompatibility with HLA class I and II alleles in persistent maternal microchimerism (MMC).1Maloney S. Smith A. Furst D.E. Myerson D. Rupert K. Evans P.C. et al.Microchimerism of maternal origin persists into adult life.J Clin Investig. 1999; 104: 41-47Crossref PubMed Scopus (373) Google Scholar Many different techniques have been used before to measure the rate of maternofetal transfusion and ME. The HLA typing of the infant having more than 50% compatibility with the mother may indicate maternal chimerism. Clinicians may use karyotype analysis if the infant is male. The test is diagnostic if the karyotype is XX in a male infant. Flow cytometry with antihuman MHC class I–specific mAbs could distinguish maternal cells from patient cells.2Müller S.M. Ege M. Pottharst A. Schulz A.S. Schwarz K. Friedrich W. Transplacentally acquired maternal T lymphocytes in severe combined immunodeficiency: a study of 121 patients.Blood. 2001; 98: 1847-1851Crossref PubMed Scopus (180) Google Scholar We can detect the chimerism via fluorescence in situ hybridization.3Hall J.M. Lingenfelter P. Adams S.L. Lasser D. Hansen J.A. Bean M.A. Detection of maternal cells in human umbilical cord blood using fluorescence in situ hybridization.Blood. 1995; 86: 2829-2832Crossref PubMed Google Scholar HLA-specific PCR could also be used.1Maloney S. Smith A. Furst D.E. Myerson D. Rupert K. Evans P.C. et al.Microchimerism of maternal origin persists into adult life.J Clin Investig. 1999; 104: 41-47Crossref PubMed Scopus (373) Google Scholar In their study, Müller et al2Müller S.M. Ege M. Pottharst A. Schulz A.S. Schwarz K. Friedrich W. Transplacentally acquired maternal T lymphocytes in severe combined immunodeficiency: a study of 121 patients.Blood. 2001; 98: 1847-1851Crossref PubMed Scopus (180) Google Scholar detected maternal cells in 48 out of 121 infants with SCID, and 19 out of 48 had clinical signs of GvHD. There are data that the maternofetal blood transfer starts in utero. MMC has been detected in fetal lymph nodes,4Mold J.E. Michaëlsson J. Burt T.D. Muench M.O. Beckerman K.P. Busch M.P. et al.Maternal alloantigens promote the development of tolerogenic fetal regulatory T cells in utero.Science. 2008; 322: 1562-1565Crossref PubMed Scopus (620) Google Scholar and it has been reported at a ratio of 23% in cord blood.5Roh E.Y. Yoon J.H. Shin S. Song E.Y. Chung H.Y. Park M.H. Frequency of fetal-maternal microchimerism: an analysis of the HLA-DRB1 gene in cord blood and maternal sample pairs.J Maternal-Fetal Neonat Med. 2017; 30: 2613-2619Crossref PubMed Scopus (9) Google Scholar Loubière et al6Loubière L.S. Lambert N.C. Flinn L.J. Erickson T.D. Yan Z. Guthrie K.A. et al.Maternal microchimerism in healthy adults in lymphocytes, monocyte/macrophages and NK cells.Lab Invest. 2006; 86: 1185-1192Crossref PubMed Scopus (111) Google Scholar showed that MMC may be seen in lymphocytes, monocyte/macrophages, and natural killer cells. There may be some factors that increase the maternofetal transfusion, such as placental infection. Maternofetal blood transfer rates during the delivery, the rate in vaginal delivery and Cesarean section, are not studied yet. Additionally maternofetal blood transfer may be through breast-feeding after the delivery.7Molès J.P. Tuaillon E. Kankasa C. Bedin A.S. Nagot N. Marchant A. et al.Breastfeeding-related maternal microchimerism.Nat Rev Immunol. 2017; 17 (729-1)Crossref PubMed Scopus (18) Google Scholar The maternal cells present in breast milk may include stem cells and progenitor cells as well as mature immune cells. Whichever way they are transferred, the maternal T and B cells will have limited diversity. Oligoclonal T cell proliferation may develop similar to Omenn syndrome. The clinical setup differs related to the characteristics of the maternal microchimeric cells. In a study, chimeric maternal cells isolated from patients with myositis were shown to react to the child's cells in vitro by producing IFN-γ.8Reed A.M. McNallan K. Wettstein P. Vehe R. Ober C. Does HLA-dependent chimerism underlie the pathogenesis of juvenile dermatomyositis?.J Immunol. 2004; 172: 5041-5046Crossref PubMed Scopus (75) Google Scholar This month Tsilifis et al9Tsilifis C. Slatter M. Cardeiro A.I. Hambleton S. Engelhardt K.R. Griffin H. et al.Congenital nephrotic syndrome in IL7Rα-SCID—a rare feature of materno-foetal graft-versus-host disease.J Allergy Clin Immunol Pract. 2021; 9: 4151-4153Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar reported a patient with SCID with congenital nephrotic syndrome accompanying maternofetal GvHD. Congenital nephrotic syndrome and hypothyroidism are the presenting features of the 3-month-old infant. Generally, the maternal cells may engraft in the thymus, heart, liver, lung, and pancreas.10Stevens A.M. Do maternal cells trigger or perpetuate autoimmune diseases in children?.Pediatr Rheumatol. 2007; 5: 1-8Crossref Scopus (16) Google Scholar Here, Tsilifis et al9Tsilifis C. Slatter M. Cardeiro A.I. Hambleton S. Engelhardt K.R. Griffin H. et al.Congenital nephrotic syndrome in IL7Rα-SCID—a rare feature of materno-foetal graft-versus-host disease.J Allergy Clin Immunol Pract. 2021; 9: 4151-4153Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar describe thyroid and kidney infiltration. Congenital hypothyroidism and nephrotic syndrome may indicate in utero infiltration of the tissues due to ME and GvHD. Although we do not routinely measure the chimerism in different tissues, the diagnosis of ME and GvHD necessitates the documentation of MMC by specific tests in blood. For the therapy, the immunosuppressives and immunomodulatory treatment may help together with the standard therapeutic approach. Microchimerism studies are on the way for evaluating immune cell development, tolerance in the offspring, and autoimmune and inflammatory diseases. Data in the last two decades have shown that MMC is not as rare as one might think. Comprehensive studies to identify chimerism will change the evaluation process of many inflammatory and autoimmune diseases. After all these data, clinicians should be ready to evaluate immunologic diseases with the grandmothers' microchimerism and MMC soon. Congenital nephrotic syndrome in IL7Rα-SCID: A rare feature of maternofetal graft-versus-host diseaseThe Journal of Allergy and Clinical Immunology: In PracticeVol. 9Issue 11PreviewBiallelic mutations in IL7R, encoding the IL-7 receptor α-chain, typically present as T−B+NK+ severe combined immunodeficiency (SCID) owing to the protein's role in early T-lymphocyte development,1 accounting for 5% to 10% of SCID cases with variation by population.2 Rarely, hypomorphic IL7R mutations may cause Omenn's syndrome (OS), manifesting as erythroderma, lymphadenopathy, hepatosplenomegaly, and raised IgE, generated by autologous autoreactive T lymphocytes.1 An important differential diagnosis is engraftment of maternal T lymphocytes causing graft-versus-host disease (maternofetal engraftment [MFE]). Full-Text PDF" @default.
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• W3211423020 title "Maternofetal Transfusion, Maternal Chimerism, and Maternal Engraftment: A Mystery in Health and Disease" @default.
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