Lymphocyte response is enhanced by supplementation of elderly subjects with selenium-enriched yeast.

PROBLEM: In normal pregnancy the maternal immune system should be directed towards tolerance or suppression in order not to reject the partly foreign feto-placental unit. The aim of this investigation was to find hallmarks of systemic immunosuppression during normal pregnancy.



METHODS: Five healthy primigravidae were examined during pregnancy and postpartum with flow cytometric analysis to define T and B lymphocyte subsets in peripheral blood. In addition, we studied the proliferative response of lymphocytes to mitogens or interleu-kin-2 (IL-2) alone or in combination with immunomodulating drugs or interleukin-4 (IL-4). The results were compared to healthy, non-pregnant women.



RESULTS: During pregnancy and early puerperium we noted an immune balance in favour of suppression, as measured by increased numbers of T “helper/suppressor” (CD4+ CD45RA+) and “suppressor”/effector T cells (CD8+S6F1-), and decreased numbers of T “helper/inducer” (CD4+CD29+), T “helper/memory” (CD4+CD45RO+), killer/effector T cells (CD8+S6F1+), and Natural Killer cells (CD56+), as well as decreased numbers of activated lymphocytes expressing IL-2 receptor (CD25+) and T cells expressing HLA-DR (HLA-DR+CD3+). During pregnancy, lymphocyte proliferation was impaired in autologous serum with concanavalin A (ConA), phytohemagglutinin (PHA), or IL-2. A difference in proliferative response to PHA or IL-2 between cultures with AB serum and autologous serum is suggestive of an immunosuppressor factor in serum during pregnancy. Indomethacin significantly increased lymphocyte proliferation in autologous serum with ConA, indicating PGE2 mediated suppressor activity during pregnancy. Chlorambucil and cimetidine modulated the proliferative response to ConA, indicating an alkylating agent sensitive and a histamine dependent suppressor activity during pregnancy.



CONCLUSIONS: During normal pregnancy, a state of systemic suppression of the maternal immune system seems to be present.

Lymphocyte subsets and mitogen stimulation of blood lymphocytes in normal pregnancy.

Hormonal and pregnancy relationships to rheumatoid arthritis: Convergent effects with immunologic and microvascular systems*

PROBLEM: The survival of the fetoplacental unit might partly depend on down-regulation of rejection reactions. Pathological maternal cellular immune response mechanisms could therefore be of pathogenic importance in pregnancies complicated by placental disorders. METHOD: A flow-cytometric analysis of T-cell subsets and B-cell, as well as serological tests for anticardioIipin antibodies (aCL), antinuclear antibodies (ANA), and rheumatoid factor (RF) were done on 90 women with complicated pregnancies. The results were compared with that of nonpregnant women (n=5), and normal pregnant women (n=5) in the third trimester. RESULTS: Two women, suffering from severe preeclampsia and eclampsia respectively, had aCL on 12 and 13 units, respectively. ANA occurred in 11 patients with moderate and severe preeclampsia and intrauterine growth retardation. All women had negative RF tests. Within the CD4 T-helper subpopulations, the proportion of suppressor/inducer T-cell population (CD4+CD45RA+) significantly increased, while the memory and helper/inducer T-cells (CD4+CD45RO+ and CD4+CD29+) significantly decreased during normal pregnancy compared to nonpregnant controls. This deviation of CD4 subpopulations was not found, or was less pronounced, in complicated pregnancies. The proportion of cytotoxic T cells (CD8+S6F1+) was significantly reduced during normal pregnancy. This reduction was less pronounced in complicated pregnancies. CONCLUSION: Systemic immunologicaI deviations toward suppression or decreased activity of the immunological response as seen in normal pregnancies, was not observed in preeclampsia, intrauterine growth retardation, intrauterine fetal death, and abruptio placentae. This lack of suppression or increased T-cell activity may have a primary pathogenic role in some women with a complicated pregnancy, or it may be second to the placental disorders

Lymphocyte Subsets and Autoantibodies in Pregnancies Complicated by Placental Disorders

Maternal immune responses during pregnancy are critical in programming the future health of a newborn. The maternal immune system is required to accommodate fetal immune tolerance as well as to provide a protective defence against infections for the immunocompromised mother and her baby during gestation and lactation. Natural immunity and antibody production by maternal B cells play a significant role in providing such immunoprotection. However, aberrations in the B cell compartment as a consequence of maternal autoimmunity can pose serious risks to both the mother and her baby. Despite their potential implication in shaping pregnancy outcomes, the role of B cells in human pregnancy has been poorly studied. This review focuses on the role of B cells and the implications of B cell depletion therapy in pregnancy. It highlights the evidence of an association between aberrant B cell compartment and obstetric conditions. It also alludes to the potential mechanisms that amplify these B cell aberrances and thereby contribute to exacerbation of some maternal autoimmune conditions and poor neonatal outcomes. Clinical and experimental evidence suggests strongly that maternal autoantibodies contribute directly to the pathologies of obstetric and neonatal conditions that have significant implications for the lifelong health of a newborn. The evidence for clinical benefit and safety of B cell depletion therapies in pregnancy is reviewed, and an argument is mounted for further clinical evaluation of B cell-targeted therapies in high-risk pregnancy, with an emphasis on improving neonatal outcomes and prevention of neonatal conditions such as congenital heart block and fetal/neonatal alloimmune thrombocytopenia.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/cei.12001

To B or not to B cells-mediate a healthy start to life.

Anti-IgM stimulation of B cells is decreased in the presence of maternal serum as compared to control media. This inhibiting influence of maternal serum is observed during the priming of the B cells. The progression of B cells into cellular proliferation was not influenced by maternal serum. At the level of the immunoglobulin secretion, the influence of maternal serum was also shown. A significant down regulation of the IgM, no change of the IgG production, and an enhanced secretion of IgA and IgE was demonstrated in the presence of maternal serum as compared to control media. It has been suggested that the maternal IgG fraction contains a molecule partly responsible for these changes. Furthermore, the CD23 antigen is increased when B cells are stimulated in the presence of a pool of maternal IgG. All the findings concerning maternal IgG were more pronounced when retroplacental IgG was used instead of peripheral maternal IgG. This observation suggests that the factor responsible for the B cell changes is ...

Modulation of B cell stimulation by maternal serum

Numerous experiments have been performed to try to explain the successful gestation of the semiallogeneic mammalian fetus in the immuno-competent mother (1, 3, 4, 5). A popular hypothesis is that localized intra uterine suppression mediates the immune response and contributes directly to the survival of the fetus (6). Suppressive factors synthesized at the fetomaternal interface may be transported by the bloodstream and be found in the retroplacental and peripheral blood circulation (7). In this report we aim to study these modulating factors by exposing a proteinaceous antigen (Candidine or human mono nuclear cells) to unrelated human lymphocytes in the presence of a pool of maternal serum, retroplacental (MAT SR) or peripheral (MAT SP), or to a pool of male or calf serum (MALS or CS).A significant downregulation of the candidine mediated lymphocytic stimulation was observed in the case of the maternal serum. In order to further characterize this inhibition, a quantitative evaluation of the expre...

Functional modifications of the CD4+ and the CD8+ subset due to maternal serum

The recent immunological literature has described the existence of a retroplacental serum factor being responsible for the downregulation of the MHC Class II antigen expression In this report, the same property has been found in peripheral maternal serum the HLA Class II modulating activity is however diminished in the presence of peripheral maternal serum as compared to retroplacental serum suggesting that the IA like inhibiting factor is released at the fetomaternal interfaceAfter a three-day incubation period of unrelated lymphocytes in a maternal serum pool, it was shown that the HLA Dr, the HLA Dp, and more significantly, the HLA Dq molecules were modulated When third party lymphocytes were stimulated by Candidine or unrelated mononuclear cells in the presence of retroplacental serum, only the cellular subpopulation belonging to the CD4+ subset showed an HLA Dq downregulation the molecular constituents of the MHC Class II antigen expression characterizing cells belonging to other sub

Modulation of the HLA class II antigen at a molecular level by maternal serum.

A retroplacental serum factor responsible for the downregulation of the MHC class II antigen expression has been described [1]. We found that maternal serum had the same property. The HLA class II modulating activity is however diminished in the presence of maternal serum as compared to retroplacental serum suggesting that the IA like inhibiting factor is released at the fetomaternal interface. After a 3-day incubation period of unrelated lymphocytes and mononuclear cord blood cells in a maternal serum pool, it was shown that the HLADr, the HLADp, and more significantly, the HLADq molecules were modulated. This phenomenon was more pronounced among cord blood cells. When third party lymphocytes and mononuclear cord blood cells were stimulated by Candidine or unrelated mononuclear cells in the presence of retroplacental serum, only the cellular subpopulation belonging to the CD4+ subset showed an HLADq downregulation. The molecular constituents of the MHC class II antigen expression characterizing cells belonging to other subsets remained unchanged. When the same stimulation assay was performed in the presence of a control medium (nulliparous serum), we found no changes in the MHC class II molecular constituents. When unrelated mononuclear cells and mononuclear cord blood cells were PHA stimulated in the presence of maternal and nulliparous serum, the HLADq expression of the CD8+ subset showed a significant downregulation in the maternal serum mediated stimulation assay as compared to the control stimulation test. The molecular expression of the HLA class II antigen related to the other subpopulation (CD4+, CD3+) stimulated by a mitogenic lectin remained unchanged. It is suggested that these molecular MHC class II modulations are due to a factor included in the maternal IgG reaction. Retroplacental IgG contains the highest concentration of this factor.

Modulation of the HLA class II antigen at a molecular level by maternal serum among cord blood cells and unrelated lymphocytes.

Neoplastic Jurkat cells were submitted to a PHA stimulation test after a preincubation in maternal or nulliparous serum (10% dilution). The Il2R expression was significantly downregulated among maternal serum treated cells.Retroplacental serum was significantly more inhibitive than peripheral maternal serum (P < 0,01). The maternal IgG fractions and mostly the retroplacental IgG fraction proved to contain a factor mainly responsible for the I12R expression inhibitive property.The molecular mechanism of this phenomenon was further studied. It was shown that H7 (acting as a protein kinase inhibitor) could not influence the Il2R modulation. E.G.T.A., a calcium chelator, was not able to interfere with the inhibitive influence of maternal serum. It was suggested that the maternal serum mediated inhibition of the IL2R expression is not influenced by the hydrolysis of membrane bound phosphatidyl inositol.In contrast, pertussis toxin markedly enhanced, in a dose dependent way, the suppressive influence of...

Mechanism of action of maternal serum on the interleukin2 receptor expression.

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