Relevant bibliographies by topics / Immune reponse/fetal effects

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Immune reponse/fetal effects'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Immune reponse/fetal effects.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Immune reponse/fetal effects"

1

Dhir, Varun. "Mesenchymal Stem Cells: The New Immunosuppressants?" Journal of Postgraduate Medicine, Education and Research 46, no. 2 (2012): 63–68. http://dx.doi.org/10.5005/jp-journals-10028-1015.

Full text
Abstract:
ABSTRACT Mesenchymal stem cells are adult stem cells which can differentiate into cells of mesodermal lineage. osteoblasts, chondroblasts and adipocytes. They have an important property of immunosuppression which is mediated mainly through soluble mediators, like interleukin-1, transforming growth factor-β, nitric oxide, indoleamine 2,3 dioxegenase, etc. They have been shown to suppress both naive and antigen experienced T cells, lead to T cell arrest, and suppress Th1 and Th17 responses. They have also been shown to lead to development of tolerogenic dendritic cells, Th2 response and expansion of T regulatory cells. Importantly, MSCs are cells with a low immunogenic potential and hence have been used both in allogenic as well as xenogenic settings. MSCs have shown efficacy in suppressing the development of autoimmune disease in various animal models, like collagen induced arthritis, MRL-lpr mice, EAE mice, etc. They have been used in small human studies, some of which have shown benefit like in systemic lupus erythematosus. Also, they have been used in graft-verus-host disease in humans with promising results. However, a single randomized controlled trial has been done and, thus, their current status remains investigational. It is hoped that they may become part of the armamentarium to control and abberant or excessive immune reponse. Key messages (1) Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate only in one lineage (mesodermal). (2) They were first discovered in the bone marrow and this remains a common source, followed by adipose tissue. There are other sources: Synovial fluid, umbilical cord blood, amniotic fluid, placenta, fetal liver. (3) MSCs are immunosuppressive, the mechanism of which is not fully elucidated, but involves action on other cells mainly through soluble mediators, like TGFβ, IDO, IL-1, NO, etc. (4) MSCs have shown efficacy in various animal models of autoimmune diseases. There have been small human studies, some of which showed benefit, however, a single randomized controlled trial has been done. (5) MSCs may have a role in autoimmune diseases refractory to treatment or as an add onto prevent treatment side effects. How to cite this article Dhir V. Mesenchymal Stem Cells: The New Immunosuppressants? J Postgrad Med Edu Res 2012;46(2):63-68.
APA, Harvard, Vancouver, ISO, and other styles
2

Zhang, Xingqi, Joanna H. Sliwowska, and Joanne Weinberg. "Prenatal Alcohol Exposure and Fetal Programming: Effects on Neuroendocrine and Immune Function." Experimental Biology and Medicine 230, no. 6 (June 2005): 376–88. http://dx.doi.org/10.1177/15353702-0323006-05.

Full text
Abstract:
Alcohol abuse is known to result in clinical abnormalities of endocrine function and neuroendocrine regulation. However, most studies have been conducted on males. Only recently have studies begun to investigate the influence of alcohol on endocrine function in females and, more specifically, endocrine function during pregnancy. Alcohol-induced endocrine imbalances may contribute to the etiology of fetal alcohol syndrome. Alcohol crosses the placenta and can directly affect developing fetal cells and tissues. Alcohol-induced changes in maternal endocrine function can disrupt maternal-fetal hormonal interactions and affect the female’s ability to maintain a successful pregnancy, thus indirectly affecting the fetus. In this review, we focus on the adverse effects of prenatal alcohol exposure on neuroendocrine and immune function, with particular emphasis on the hypothalamic-pituitary-adrenal (HPA) axis and the concept of fetal programming. The HPA axis is highly susceptible to programming during fetal development. Early environmental experiences, including exposure to alcohol, can reprogram the HPA axis such that HPA tone is increased throughout life. We present data that demonstrate that maternal alcohol consumption increases HPA activity in both the maternal female and the offspring. Increased exposure to endogenous glucocorticoids throughout the lifespan can alter behavioral and physiologic responsiveness and increase vulnerability to illnesses or disorders later in life. Alterations in immune function may be one of the long-term consequences of fetal HPA programming. We discuss studies that demonstrate the adverse effects of alcohol on immune competence and the increased vulnerability of ethanol-exposed offspring to the immunosuppressive effects of stress. Fetal programming of HPA activity may underlie some of the long-term behavioral, cognitive, and immune deficits that are observed following prenatal alcohol exposure.
APA, Harvard, Vancouver, ISO, and other styles
3

Saito, Mika, Earl Silverman, Fraser Golding, Vitor Guerra, Linda Hiraki, Varsha Thakur, and Edgar Jaeggi. "Effects of Transplacental Dexamethasone Therapy on Fetal Immune-Mediated Complete Heart Block." Fetal Diagnosis and Therapy 48, no. 3 (2021): 183–88. http://dx.doi.org/10.1159/000513202.

Full text
Abstract:
<b><i>Introduction:</i></b> Antibody-mediated complete atrioventricular block (CAVB) is considered irreversible. We sought to examine the effects of transplacental steroids on fetal AV conduction. <b><i>Methods:</i></b> Fifty-nine fetuses diagnosed with CAVB at our center from 1996 to 2018 were reviewed. Routine dexamethasone administration to birth was used to limit cardiac inflammatory damage. Restoration of fetal AV conduction was classified as “unexpected” treatment response. <b><i>Results:</i></b> CAVB resolved in 5/29 (17%) fetuses first treated ≤24-week gestation with 8 mg/day of dexamethasone, when compared with 0/30 (0%) when treatment was initiated later and/or at a starting dose of 4 mg/day (odds ratio 13.69; 95% confidence interval 0.72–260.13; <i>p</i> = 0.024). Treatment response was also associated with a faster ventricular rate at diagnosis (median [range]: 80 [60–97] beats per minute [bpm] vs. 58 [38–92] bpm; <i>p</i> = 0.0036). CAVB reappeared in all 5 responders either prenatally (<i>n</i> = 1) or postnatally before (<i>n</i> = 3) or after (<i>n</i> = 1) the first year of life. When compared with infants with treatment-resistant CAVB (median follow-up 10.3 years), responders (median follow-up 12.3 years) required postnatal pacing less frequent (2/5 [40%] vs. 45/49 [92%]; <i>p</i> = 0.013). <b><i>Conclusions:</i></b> In a subgroup of CAVB fetuses, dexamethasone transiently restored AV conduction. This was associated with a lower rate of postnatal pacing when compared with nonresponders.
APA, Harvard, Vancouver, ISO, and other styles
4

Ghanmi, Z., M. Rouabhia, O. Othmane, and P. A. Deschaux. "5.3 Effects of metal ions on cyprinid fish immune response: in vitro effects of Zn2+ and Mn2+ on the mitogenic reponse of carp pronephros lymphocytes." Developmental & Comparative Immunology 13, no. 4 (September 1989): 398. http://dx.doi.org/10.1016/0145-305x(89)90115-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Childs, Caroline E., Tessa Romijn, Uta Enke, Samuel Hoile, and Philip C. Calder. "Maternal diet during pregnancy has tissue-specific effects upon fetal fatty acid composition and alters fetal immune parameters." Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) 83, no. 4-6 (October 2010): 179–84. http://dx.doi.org/10.1016/j.plefa.2010.08.007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Arneth, Borros. "Neonatal Immune Incompatibilities between Newborn and Mother." Journal of Clinical Medicine 9, no. 5 (May 14, 2020): 1470. http://dx.doi.org/10.3390/jcm9051470.

Full text
Abstract:
Background: Incompatibilities between the mother and unborn baby can cause complications that must be identified early to initiate the appropriate treatment. For example, neonatal alloimmune thrombocytopenia (NAIT), neonatal alloimmune neutropenia (NAIN), and morbus hemolyticus neonatorum affect children worldwide. Aim: This literature review aims to depict the similarities and differences between these three disorders from a clinical and mechanistic point of view. Material and Methods: The current literature review entailed conducting a systematic search to locate articles on the three conditions. Different electronic databases, including PsycINFO, PubMed, Web of Science, and CINAHL, were searched using the search terms “neonatal alloimmune thrombocytopenia”, “neonatal alloimmune neutropenia”, “morbus hemolyticus neonatorum”, “NAIT”, “FNAIT”, “fetal”, “NAIN”, and “hemolytic disease of the newborn”. Results: This review shows that these three diseases are caused by incompatibilities between the maternal and fetal immune systems. Furthermore, these conditions can lead to severe complications that hinder fetal development and cause death if not well managed. Discussion: The current literature review shows that NAIT, NAIN, and morbus hemolyticus neonatorum are rare conditions that occur when the mother produces antibodies against the fetal immune system. Thus, there is a need for the early detection of these conditions to initiate appropriate treatment before the child experiences adverse effects. Conclusion: The development of NAIT, NAIN, and morbus hemolyticus neonatorum is linked to the production of antibodies against the fetal immune system and fetal antigens. Further studies are required to determine potential interventions to reduce the risk of developing these three conditions.
APA, Harvard, Vancouver, ISO, and other styles
7

Garbett, K. A., E. Y. Hsiao, S. Kálmán, P. H. Patterson, and K. Mirnics. "Effects of maternal immune activation on gene expression patterns in the fetal brain." Translational Psychiatry 2, no. 4 (April 2012): e98-e98. http://dx.doi.org/10.1038/tp.2012.24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ehninger, Dan. "Tsc2Haploinsufficiency Has Limited Effects on Fetal Brain Cytokine Levels during Gestational Immune Activation." Autism Research and Treatment 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/761279.

Full text
Abstract:
Dysregulated TSC/mTOR signaling may play a pathogenetic role in forms of syndromic autism, such as autism associated with tuberous sclerosis, a genetic disorder caused by heterozygousTSC1orTSC2mutations. Environmental risk factors, such as gestational viral infections, may, in some cases, also contribute to the pathogenesis of autism and related neuropsychiatric disorders. We have recently found that a heterozygousTsc2mutation and the poly I:C model of maternal immune activation (MIA) interactively perturb fetal development and adult social behavior in mice, suggesting that these factors converge on shared pathways. TSC/mTOR signaling plays an important role in the modulation of immune responses, raising the possibility that the damage caused by MIA was greater inTsc2+/−than in wildtype fetuses because of an exacerbated immune response in the mutants. Here, cytokine antibody arrays were employed to measure relative cytokine abundances in the fetal brain and the placenta during MIA. Cytokines were induced by gestational poly I:C but there was no obvious modulatory effect ofTsc2haploinsufficiency. The data indicate that cytokine exposure during MIA is comparable inTsc2haploinsufficient and wildtype control fetuses, suggesting that downstream molecular and cellular processes may account for the interactive effects ofTsc2haploinsufficiency and MIA.
APA, Harvard, Vancouver, ISO, and other styles
9

McLaurin, J., JP Antel, and VW Yong. "Immune and non-immune actions of interferon-β-1b on primary human neural cells." Multiple Sclerosis Journal 1, no. 1 (April 1995): 10–19. http://dx.doi.org/10.1177/135245859500100103.

Full text
Abstract:
Systemic interferon-β-1b (IFN-β-1b) reduces the frequency of clinical exacerbations and the number of magnetic resonance imaging (MRI)-defined lesions in patients with relapsing—remitting MS. The basis for this clinical effect is not understood. While IFN-β-1b has been demonstrated to have antiproliferative and immunomodulatory effects on the sytemic immune system, its actions on neural cells could also contribute to its therapeutic efficacy. In this study, we hove examined possible immune and non-immune effects of IFN-β-1b on CNS-derived primary human cells. With respect to immune-related effects, application of IFN-β-1b did not decrease basal expression of HLA-DR on astrocytes or microglia, and it reduced the IFN-γ-enhanced HLA-DR expression on adult human astrocytes only at high concentrations (1000 IU ml-1); IFN-β-1b at all concentrations tested did not reduce the IFN-γ-enhanced HLA-DR expression by fetal astrocytes or adult microglial cells. In contrast, but in correspondence with the literature, the IFN-γ-enhanced HLA-DR expression on a glioma cell line was attenuated by IFN-β-1b in a dose-dependent manner. With respect to non-immune effects, the number of adult human oligodendrocytes and their state of morphological differentiation were not affected by IFN-β-1b. Proliferation of the mitotically active fetal human astrocytes, however, was reduced by IFN-β-1b treatment Lactate dehydrogenase assays revealed that IFN-β-1b was not toxic to neural cells, including adult oligodendrocytes and fetal human neurons. We conclude that IFN-β-1b lacks efficacy in down-regulating HLA-DR expression by primary human neural cells and that regulation of MHC class II antigens is unlikely to be a mechanism for its beneficial effect in MS. Finally, the lack of toxicity of IFN-β-1b on human neural cells is important for a drug that will probably be used widely.
APA, Harvard, Vancouver, ISO, and other styles
10

Knapek, Katie J., Hanah M. Georges, Hana Van Campen, Jeanette V. Bishop, Helle Bielefeldt-Ohmann, Natalia P. Smirnova, and Thomas R. Hansen. "Fetal Lymphoid Organ Immune Responses to Transient and Persistent Infection with Bovine Viral Diarrhea Virus." Viruses 12, no. 8 (July 28, 2020): 816. http://dx.doi.org/10.3390/v12080816.

Full text
Abstract:
Bovine Viral Diarrhea Virus (BVDV) fetal infections occur in two forms; persistent infection (PI) or transient infection (TI), depending on what stage of gestation the fetus is infected. Examination of lymphoid organs from both PI and TI fetuses reveals drastically different fetal responses, dependent upon the developmental stage of the fetal immune system. Total RNA was extracted from the thymuses and spleens of uninfected control, PI, and TI fetuses collected on day 190 of gestation to test the hypothesis that BVDV infection impairs the innate and adaptive immune response in the fetal thymus and spleen of both infection types. Transcripts of genes representing the innate immune response and adaptive immune response genes were assayed by Reverse Transcription quatitative PCR (RT-qPCR) (2−ΔΔCq; fold change). Genes of the innate immune response, interferon (IFN) inducible genes, antigen presentation to lymphocytes, and activation of B cells were downregulated in day 190 fetal PI thymuses compared to controls. In contrast, innate immune response genes were upregulated in TI fetal thymuses compared to controls and tended to be upregulated in TI fetal spleens. Genes associated with the innate immune system were not different in PI fetal spleens; however, adaptive immune system genes were downregulated, indicating that PI fetal BVDV infection has profound inhibitory effects on the expression of genes involved in the innate and adaptive immune response. The downregulation of these genes in lymphocytes and antigen-presenting cells in the developing thymus and spleen may explain the incomplete clearance of BVDV and the persistence of the virus in PI animals while the upregulation of the TI innate immune response indicates a more mature immune system, able to clear the virus.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Immune reponse/fetal effects"

1

Arkwright, P. D. "Effects of the human trophoblast on lymphocyte proliferation." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236250.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Chen, Huang-Tsu. "Identification of bovine growth hormone receptor in fetal lymphoid cells and effects of growth hormone on fetal immune development and function." 1996. http://catalog.hathitrust.org/api/volumes/oclc/36864503.html.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Immune reponse/fetal effects"

1

Coyle, Patricia K. Immune-mediated Disorders of the Central Nervous System. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0010.

Full text
Abstract:
This chapter reviews pregnancy in multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and acute transverse myelitis (ATM) syndrome. MS is a major acquired disease of young adults, with a rising female predominance. MS has no direct negative consequences on fertility or pregnancy. Pregnancy has a profound effect on MS, with decrease in disease activity during the last trimester counteracted by a three-month postpartum increase in disease activity. With the development of disease-modifying therapies, important questions arise about washout periods, the feasibility and risks of treating during pregnancy and breastfeeding, and the potential of treatment-related adverse fetal effects. Fortunately, there is good information to counsel women with MS. Neuromyelitis Optica Spectrum Disorder (NMOSD) is a neuroimmune channelopathy. It is a distinct disorder from MS. NMOSD disease activity is not favorably affected by pregnancy. The postpartum period has real risk for disabling attacks. This influences recommendations about breastfeeding and how quickly to resume therapy postpartum. Acute transverse myelitis (ATM) syndrome can occur in both MS and NMOSD but can also be due to other disorders. Workup and treatment of ATM during pregnancy is reviewed, as well as implications for delivery.
APA, Harvard, Vancouver, ISO, and other styles
2

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin D in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0015.

Full text
Abstract:
Vitamin D, which is synthesized in skin exposed to UV light, or is consumed in the diet, plays a key role in maintaining bone integrity via the regulation of calcium and phosphorus homeostasis. It also influences a number of extra-skeletal processes, including immune function and blood glucose homeostasis. Maternal vitamin D deficiency in pregnancy leads to poor fetal skeletal mineralization in utero that can manifest as rickets in newborns. In addition to skeletal effects, women with very low vitamin D status face increased risks of other adverse pregnancy outcomes and possible long-term effects on their own health and that of their offspring. However, controversy remains over definitions of vitamin D sufficiency and deficiency, complicating recommendations on maternal intakes. At a minimum, all pregnant women should take a supplement of 400 IU/day, in addition to sensible sun exposure and increasing their intake of food sources.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Immune reponse/fetal effects"

1

Impey, Lawrence. "Fetal effects of maternal infection." In Oxford Textbook of Medicine, edited by Catherine Nelson-Piercy, 2678–86. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0278.

Full text
Abstract:
This chapter looks at the fetal effects of maternal infection. Immunity is mildly suppressed in pregnancy, and the fetal immune system is developmentally immature. Infections in pregnancy can therefore be devastating both for the mother, as is occasionally seen with varicella, and for the fetus, as exemplified by congenital infections such as those caused by rubella, cytomegalovirus, syphilis, and toxoplasmosis. The fetal effects of maternal infection in pregnancy can be broadly categorized as follows (these are not mutually exclusive): transplacental infection causing fetal malformation (e.g. treponema pallidum, rubella); transplacental infection causing severe in utero illness (e.g. parvovirus); neonatal infection/carrier status as a result of transplacental or intrapartum infection (e.g. HIV, herpes zoster); such neonatal infection may be severe; preterm delivery, late miscarriage, perinatal death, and cerebral palsy at term delivery are more common in the presence of in utero and placental infection (chorioamnionitis) (e.g. group B streptococcus).
APA, Harvard, Vancouver, ISO, and other styles
2

Azamor, Tamiris, Amanda Torrentes-Carvalho, Zilton Vasconcelos, Ana Paula Dinis Ano Bom, and Juliana Gil Melgaço. "Innate Immunity Modulation during Zika Virus Infection on Pregnancy: What We Still Need to Know for Medical Sciences Breakthrough." In Cell Interaction - Molecular and Immunological Basis for Disease Management. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.94861.

Full text
Abstract:
Zika virus (ZIKV), an arthropod-borne flavivirus, was classified as reemerging infectious disease and included as neglected tropical disease. During the recent ZIKV outbreak in South America, it has been demonstrated that ZIKV infection during pregnancy is strongly associated with fetal loss, malformations and neurological disorders in newborns. Despite the first line of host immune defense is related to innate immunity activation, the immunological homeostasis is essential for pregnancy success. Although the dynamic changes in maternal-fetal immunity is not completely understood and poorly investigated, the knowledge of immune responses during gestation is very important for infectious disease prevention and control, as ZIKV. Here, we put together more and new information about the innate immunity during gestation, highlighting three parts probably involved with clinical outcome and/or not well explored in literature: 1) type III interferon; 2) innate regulatory cells; and 3) cell death pathways modulation. Additionally, we will be focused on discussing how the dynamic responses of innate immune system during pregnancy and its effects in newborns, could be modulated by ZIKV, as well as how efforts on development of new/old drugs and vaccines could be effective for ZIKV prevention and control to provide a successful pregnancy.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Immune reponse/fetal effects' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography