Увійти

Готові списки джерел за темами / Neonatal immune tolerance

Добірка наукової літератури з теми "Neonatal immune tolerance"

Автор: Grafiati

Опубліковано: 15 вересня 2021

Оновлено: 9 лютого 2022

Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями

Оберіть тип джерела:

Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Neonatal immune tolerance".

Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.

Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.

Зміст

Статті в журналах
Дисертації
Частини книг

Статті в журналах з теми "Neonatal immune tolerance":

1

Tai, Denise S., Chuhong Hu, and Gerald S. Lipshutz. "Immune tolerance induction with neonatal gene therapy." Journal of the American College of Surgeons 217, no. 3 (September 2013): S136. http://dx.doi.org/10.1016/j.jamcollsurg.2013.07.316.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

2

Shi, Yimin, Rustom Falahati, and Karin ML Gaensler. "Tolerance Induction by Neonatal Gene Delivery." Blood 112, no. 11 (November 16, 2008): 4628. http://dx.doi.org/10.1182/blood.v112.11.4628.4628.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract Advances in the design and efficiency of gene delivery vectors have enabled the initiation of clinical trials in gene therapy for genetic and other disorders. However, the development of inhibitory immune responses to vector antigens and to therapeutic proteins remains an obstacle. Efforts to limit these immune responses by immunosuppressive and immuno-modulatory approaches have met with limited success. Our approach is to deliver and express viral vectors early in immune ontogeny and thereby induce immune tolerance to both vectors and therapeutic proteins. We have previously shown that in utero delivery of AAV-2 vectors produces lifelong gene expression without immune responses, and that augmented levels of gene expression are achieved with re-administration of AAV vectors. Because fetal injections are limited by technical issues, our current focus is to use a neonatal model for defining the critical period when tolerance to vector and transgene may be achieved by primary injection. We are also exploring mechanisms of tolerance induction to neo-antigens. We have delivered AAV serotypes 1 and 8 with higher transduction efficiencies than AAV-2, to assess the expression levels, duration, and tissue distribution of luciferase by semi-quantitative longitudinal in vivo bioluminescence assays. In both C57BL/6 and BALB/c strains, neonatal injection of AAV1-Luc or AAV8-Luc by either IP, IV or IT routes produces lifelong gene expression. After IP injection at day 1–2 of life, gene expression increases 10–20 fold over the next several months. Highest levels of expression were achieved by IP injection, with lowest levels observed after IV injection. Injection of AAV1-Luc achieved higher levels of luciferase expression than did injection of AAV8- Luc. In contrast to the localized distribution of AAV1 mediated luciferase expression in the injected area, widespread, systemic expression of luciferase mediated by AAV8 after neonatal delivery is observed, regardless of the route of delivery. The effect of this altered tropism on gene expression levels and tolerance induction is being examined. In both C57BL/6 and BALB/c mice, IP injection of AAV1-Luc or AAV8-Luc at 1–2 days, 1 week, 2 weeks, or 3 weeks of age produced lifelong expression of luciferase and resulted in increasing levels of antibody responses against AAV1 or AAV8 with increasing age at primary injection. Antibody titers to AAV1 or AAV8 in animals injected at day 1–2 of life were comparable to background levels in uninjected animals. In C57BL/6 mice receiving a primary injection of AAV8-Luc, secondary injection of AAV8-Luc boosted the antibody response to AAV8 in the animals first injected at 1 week, 2 weeks or 3 weeks, but not in the animals injected at 1–2 day of life. We are currently exploring whether augmented expression with re-administration of AAV vectors in adult animals is due to an active process such as tolerance, partial tolerance or anergy. Developing strategies for the induction of tolerance to gene delivery vectors and therapeutic gene products will be an important advance for gene therapy for genetic and other disorders.

3

Ohsaki, Asa, Nicholas Venturelli, Tess M. Buccigrosso, Stavroula K. Osganian, John Lee, Richard S. Blumberg, and Michiko K. Oyoshi. "Maternal IgG immune complexes induce food allergen–specific tolerance in offspring." Journal of Experimental Medicine 215, no. 1 (November 20, 2017): 91–113. http://dx.doi.org/10.1084/jem.20171163.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

The role of maternal immune responses in tolerance induction is poorly understood. To study whether maternal allergen sensitization affects offspring susceptibility to food allergy, we epicutaneously sensitized female mice with ovalbumin (OVA) followed by epicutaneous sensitization and oral challenge of their offspring with OVA. Maternal OVA sensitization prevented food anaphylaxis, OVA-specific IgE production, and intestinal mast cell expansion in offspring. This protection was mediated by neonatal crystallizable fragment receptor (FcRn)–dependent transfer of maternal IgG and OVA immune complexes (IgG-IC) via breast milk and induction of allergen-specific regulatory T (T reg) cells in offspring. Breastfeeding by OVA-sensitized mothers or maternal supplementation with IgG-IC was sufficient to induce neonatal tolerance. FcRn-dependent antigen presentation by CD11c+ dendritic cells (DCs) in offspring was required for oral tolerance. Human breast milk containing OVA-IgG-IC induced tolerance in humanized FcRn mice. Collectively, we demonstrate that interactions of maternal IgG-IC and offspring FcRn are critical for induction of T reg cell responses and control of food-specific tolerance in neonates.

4

Nivsarkar, Megha S., Suzanne M. K. Buckley, Alan L. Parker, Dany Perocheau, Tristan R. McKay, Ahad A. Rahim, Steven J. Howe, and Simon N. Waddington. "Evidence for Contribution of CD4+CD25+ Regulatory T Cells in Maintaining Immune Tolerance to Human Factor IX following Perinatal Adenovirus Vector Delivery." Journal of Immunology Research 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/397879.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Following fetal or neonatal gene transfer in mice and other species immune tolerance of the transgenic protein is frequently observed; however the underlying mechanisms remain largely undefined. In this study fetal and neonatal BALB/c mice received adenovirus vector to deliver human factor IX (hFIX) cDNA. The long-term tolerance of hFIX was robust in the face of immune challenge with hFIX protein and adjuvant but was eliminated by simultaneous administration of anti-CD25+ antibody. Naive irradiated BALB/c mice which had received lymphocytes from donors immunised with hFIX developed anti-hFIX antibodies upon immune challenge. Cotransplantation with CD4+CD25+ cells isolated from neonatally tolerized donors decreased the antibody response. In contrast, cotransplantation with CD4+CD25− cells isolated from the same donors increased the antibody response. These data provide evidence that immune tolerance following perinatal gene transfer is maintained by a CD4+CD25+ regulatory population.

5

Mattis, Virginia B., Dustin R. Wakeman, Colton Tom, Hemraj B. Dodiya, Sylvia Y. Yeung, Andrew H. Tran, Ksenija Bernau, et al. "Neonatal immune-tolerance in mice does not prevent xenograft rejection." Experimental Neurology 254 (April 2014): 90–98. http://dx.doi.org/10.1016/j.expneurol.2014.01.007.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

6

Černý, Viktor, Olga Novotná, Petra Petrásková, Kateřina Hudcová, Kristýna Boráková, Ludmila Prokešová, Libuše Kolářová, and Jiří Hrdý. "Lower Functional and Proportional Characteristics of Cord Blood Treg of Male Newborns Compared with Female Newborns." Biomedicines 9, no. 2 (February 9, 2021): 170. http://dx.doi.org/10.3390/biomedicines9020170.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Understanding the early events involved in the induction of immune tolerance to harmless environmental antigens and microbiota compounds could reveal potential targets for allergic disease therapy or prevention. Regulatory T cells (Treg), particularly induced Treg (iTreg), are crucial for the induction and maintenance of tolerance against environmental antigens including allergens. A decrease in the number and/or function of Treg or iTreg could represent an early predictor of allergy development. We analyzed proportional and functional properties of Treg in the cord blood of children of allergic mothers (neonates at high risk of allergy development) and healthy mothers (neonates with relatively low risk of allergy development). We observed a higher number of induced Treg in the cord blood of females compared to males, suggesting an impaired capacity of male immunity to set up tolerance to allergens, which could contribute to the higher incidence of allergy observed in male infants. The decreased proportion of iTreg in cord blood compared with maternal peripheral blood documents the general immaturity of the neonatal immune system. We observed a positive correlation in the demethylation of the Treg-specific demethylated region (TSDR) and the proportion of Treg in cord blood. Our data suggest that immaturity of the neonatal immune system is more severe in males, predisposing them to increased risk of allergy development.

7

Secher, Thomas, Delphine Payros, Camille Brehin, Michele Boury, Claude Watrin, Marion Gillet, Isabelle Bernard-Cadenat, et al. "Oral Tolerance Failure upon Neonatal Gut Colonization with Escherichia coli Producing the Genotoxin Colibactin." Infection and Immunity 83, no. 6 (March 30, 2015): 2420–29. http://dx.doi.org/10.1128/iai.00064-15.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

The intestinal barrier controls the balance between tolerance and immunity to luminal antigens. When this finely tuned equilibrium is deregulated, inflammatory disorders can occur. There is a concomitant increase, in urban populations of developed countries, of immune-mediated diseases along with a shift inEscherichia colipopulation from the declining phylogenetic group A to the newly dominant group B2, including commensal strains producing a genotoxin called colibactin that massively colonized the gut of neonates. Here, we showed that mother-to-offspring early gut colonization by colibactin-producingE. coliimpairs intestinal permeability and enhances the transepithelial passage of luminal antigen, leading to an increased immune activation. Functionally, this was accompanied by a dramatic increase in local and systemic immune responses against a fed antigen, decreased regulatory T cell population, tolerogenic dendritic cells, and enhanced mucosal delayed-type hypersensitivity response. Conversely, the abolition of colibactin expression by mutagenesis abrogates the alteration of oral tolerance induced by neonatal colonization byE. coli. In conclusion, the vertical colonization byE. coliproducing the genotoxin colibactin enhances intestinal translocation and subsequently alters oral tolerance. Thus, early colonization byE. colifrom the newly dominant phylogenetic group B2, which produces colibactin, may represent a risk factor for the development of immune-mediated diseases.

8

Elahi, Shokrollah. "Neonatal and Children’s Immune System and COVID-19: Biased Immune Tolerance versus Resistance Strategy." Journal of Immunology 205, no. 8 (August 21, 2020): 1990–97. http://dx.doi.org/10.4049/jimmunol.2000710.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

9

Matsui, Hideto, Masaru Shibata, Brian Brown, Andrea Labelle, Carol Hegadorn, Chandler Andrews, Marinee Chuah, et al. "A murine model for induction of long-term immunologic tolerance to factor VIII does not require persistent detectable levels of plasma factor VIII and involves contributions from Foxp3+ T regulatory cells." Blood 114, no. 3 (July 16, 2009): 677–85. http://dx.doi.org/10.1182/blood-2009-03-202267.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract Under certain instances, factor VIII (FVIII) stimulates an immune response, and the resulting neutralizing antibodies present a significant clinical challenge. Immunotherapies to re-establish or induce long-term tolerance would be beneficial, and an in-depth knowledge of mechanisms involved in tolerance induction is essential to develop immune-modulating strategies. We have developed a murine model system for studying mechanisms involved in induction of immunologic tolerance to FVIII in hemophilia A mice. We used lentiviral vectors to deliver the canine FVIII transgene to neonatal hemophilic mice and demonstrated that induction of long-term FVIII tolerance could be achieved. Hemophilia A mice are capable of mounting a robust immune response to FVIII after neonatal gene transfer, and tolerance induction is dependent on the route of delivery and type of promoter used. High-level expression of FVIII was not required for tolerance induction and, indeed, tolerance developed in some animals without evidence of detectable plasma FVIII. Tolerance to FVIII could be adoptively transferred to naive hemophilia recipient mice, and FVIII-stimulated splenocytes isolated from tolerized mice expressed increased levels of interleukin-10 and decreased levels of interleukin-6 and interferon-γ. Finally, induction of FVIII tolerance mediated by this protocol is associated with a FVIII-expandable population of CD4+CD25+Foxp3+ regulatory T cells.

10

Tourneur, Emilie, and Cecilia Chassin. "Neonatal Immune Adaptation of the Gut and Its Role during Infections." Clinical and Developmental Immunology 2013 (2013): 1–17. http://dx.doi.org/10.1155/2013/270301.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

The intestinal tract is engaged in a relationship with a dense and complex microbial ecosystem, the microbiota. The establishment of this symbiosis is essential for host physiology, metabolism, and immune homeostasis. Because newborns are essentially sterile, the first exposure to microorganisms and environmental endotoxins during the neonatal period is followed by a crucial sequence of active events leading to immune tolerance and homeostasis. Contact with potent immunostimulatory molecules starts immediately at birth, and the discrimination between commensal bacteria and invading pathogens is essential to avoid an inappropriate immune stimulation and/or host infection. The dysregulation of these tight interactions between host and microbiota can be responsible for important health disorders, including inflammation and sepsis. This review summarizes the molecular events leading to the establishment of postnatal immune tolerance and how pathogens can avoid host immunity and induce neonatal infections and sepsis.

Більше джерел

Дисертації з теми "Neonatal immune tolerance":

1

Li, Shuang. "Molecular mechanisms leading to the emergence of mouse regulatory T lymphocytes specific to non-inherited maternal antigens." Doctoral thesis, Universite Libre de Bruxelles, 2021. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/327043.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

[EN]It is well illustrated that the generation of Tregs is the main mechanism responsible for maintaining immune tolerance during developmental exposure to non-inherited maternal antigen (NIMA). Moreover, the presence of NIMA-specific Tregs in the uterus of pregnant mice promote reproductive fitness by enforcing maternal tolerance to overlapping paternal antigens expressed by the fetus during next-generation pregnancies. However, the reason why perinatal T cell lineage is biased towards immune tolerance is poorly understood. Due to the fact that terminal deoxynucleotidyl transferase (TdT) is not expressed in neonatal T cells in the mouse, neonatal T cells have a less diverse TCR repertoire. This is known to limit their specificity and to increase their affinity for MHC/peptide complexes. At the start of the present work, we postulated that expressing high affinity TCR might be the reason that forces the development of antigen-specific Tregs in neonates. We undertook our study with the aim to investigate the mechanisms underlying mouse NIMA-specific Treg development in the perinatal period. Using 2W1S-OVA+ heterozygous mouse model in which 2W1S antigen was transformed into surrogate NIMA for half of the offspring, we observed an increased frequency of 2W1S-specific Tregs in NIMA-2W1S-exposed animals. Moreover, we also observed that periphery-derived NIMA-2W1S Tregs had a less diverse TCR repertoire and were phenotypically distinct from thymus-derived SELF-2W1S-specific Tregs. In order to investigate whether the lack of diversity was responsible for the development of neonatal NIMA-specific Tregs, we generated transgenic mice where TdT expression was enforced in T cells before birth. We found that transgenic TdT added clonal TCR diversity but did not prevent the development of T cell clones with neonatal type TCR repertoire and did not modify the frequency of neonatal NIMA-specific Tregs. On the contrary, TdT expression increased significantly generation of SELF-specific Tregs to levels similar to that of NIMA-specific Tregs. Taken together, our data indicate that the developmental pathways of NIMA- and SELF-specific Treg repertoire are different in terms of inducing and maintaining neonatal tolerance.
[FR]Il est bien illustré que la génération périnatal de Treg est le principal mécanisme responsable du maintien de la tolérance immunitaire fœtale qui se développe suite à l'exposition aux antigènes maternels non-hérités (NIMA). De plus, la présence de Tregs spécifiques des NIMA dans l'utérus des femmes enceintes favorise la capacité de reproduction en renforçant la tolérance maternelle aux mêmes antigènes paternels exprimés par le fœtus pendant les grossesses de prochaine génération. Cependant, la raison pour laquelle la lignée des cellules T fœtales est biaisée en faveur de la tolérance immunitaire est mal comprise. Chez la souris, en raison du manque d'expression de la désoxynucléotidyl transférase terminale (TdT), les cellules T néonatales ont un répertoire de TCR moins diversifié. Ceci est connu pour limiter leur spécificité et augmenter leur affinité pour les complexes CMH / peptide. Au début du présent travail, nous avons émis l'hypothèse que l'expression de TCRs de haute affinité pourrait être la raison qui force le développement de Treg spécifiques chez les nouveau-nés. Nous avons plus particulièrement entrepris notre étude dans le but d'étudier les mécanismes sous-jacents au développement de Tregs spécifiques des NIMA chez la souris pendant la période périnatale. En utilisant le modèle de souris hétérozygotes pour 2W1S-OVA+ dans lequel l'antigène 2W1S a été transformé en NIMA pour la moitié de la progéniture, nous avons observé une fréquence accrue de Tregs spécifiques de 2W1S chez les animaux exposés au NIMA. De plus, nous avons également observé que les Treg NIMA-2W1S dérivés de la périphérie avaient un répertoire de TCRs moins diversifié et étaient phénotypiquement distincts des Tregs spécifiques de SELF-2W1S dérivés du thymus. Afin de déterminer si le manque de diversité était responsable du développement de Tregs néonataux spécifiques de NIMA, nous avons généré des souris transgéniques où l'expression de TdT était appliquée dans les cellules T avant la naissance. Nous avons constaté que le TdT transgénique ajoutait une diversité de TCR clonale, mais n'empêchait pas le développement de clones de cellules T avec un répertoire TCR de type néonatal et ne modifiait pas la fréquence des Treg néonataux spécifiques du NIMA. Au contraire, l'expression de TdT a augmenté de manière significative la génération de Tregs spécifiques de SELF-2W1S à des niveaux similaires à ceux des Treg spécifiques de NIMA-2W1S. Prises ensembles, nos données indiquent que les voies de développement du répertoire des Tregs néonataux spécifiques de NIMA et SELF sont différentes en termes d'induction et de maintien de la tolérance néonatale.
Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished

2

Porubská, Bianka. "Studium mechanizmů přežívání Sertoliho buněk v xenogenním organizmu." Master's thesis, 2018. http://www.nusl.cz/ntk/nusl-388393.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Sertoli cells (SCs) are somatic cells located in the testes. They are the only cells in direct contact with germ cells and play a key role in process of spermatogenesis. New insights in the biology of SCs are highlighting the immunological function of these cells: germ cells protection by maintaining the immunoprotective niche, creating the blood- testis barrier and local modulation of the immune response to spermatic cells. Immunomodulatory activity of SCs is preserved after their allo- and xenogeneic transplantation, and thus SCs prolongs survival not only of themselves but also of cells transplanted with them. The aim of this thesis was to study the survival and migration of SCs precursors (TSC) in mice recipients. The project is employing the neonatal tolerance phenomenon and evolutionary distinct donor organism, Xenopus tropicalis, to monitor conserved mechanisms of immune system (IS) modulation using SCs. SCs were detectable in the lungs and thymus 7 days after transplantation. The phenotype of immune cells was not altered 30 days after transplantation, however we detected changes in cytokine environment, namely increased levels of cytokines typical for Th2 and Treg immune responses. In vitro experiments further confirmed IS modulation by SCs - changing the phenotype of macrophages to alternatively...

Частини книг з теми "Neonatal immune tolerance":

1

Aulanniam, Aulanni’am, Zulkarnain Zulkarnain, Djoko Wahono Soeatmadji, Dyah Kinasih Wuragil, and Yudit Oktanella. "Thyroid Peroxidase (TPO) and Thyroid Stimulating Hormone Receptor (TSHR) Based Detection on Grave for Pregnant Women." In Graves' Disease [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96509.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Graves’ disease is a form of specific autoimmune disorder in the thyroid organ characterized by thyroid-stimulating antibodies (TSAb). Pregnant women are the most susceptible to GD due to hormonal changes and tolerance of immune responses during pregnancy. The incidence of prematurity, low birth weight (LBW), and neonatal thyrotoxicosis risk are the most complications that can be acquired if treatment is late and inadequate. It has implications for increased fetomaternal morbidity and mortality. Apart from being a biomarker for definitive diagnosis, TSAb testing is also beneficial for assessing treatment response and predicting relapse of GD (relapse) after oral anti-thyroid treatment. GD patients with high TPOAb titers also tend to have a high relapse rate. However, the evaluation of both TSAb and TPOAb examinations during and after treatment is rarely done routinely due to the examination’s high cost. This works proposed developing TSHR and TPO antigen-based rapid diagnostic tests through the immunochromatography method to address the challenges of financing and limited laboratory facilities in the area. Besides, understanding the importance of examining thyroid antibodies (TSAb and TPOAb) and interpretation in clinical practice is still a matter of debate in clinical circles, so it requires in-depth information.

2

Matyas, Melinda. "Preterm Birth and Inflammation." In Caesarean Section [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96970.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Half of all preterm births are caused or triggered by an inflammation at fetal-maternal interface. The sustained inflammation that preterm neonates are exposed is generated by maternal chorioamnionitis, premature rupture of membranes. This inflammation will facilitate the preterm labor, but also plays an important role in development of disease like: bronchopulmonary dysplasia, necrotizing enterocolitis, retinopathy of prematurity, intraventricular hemorrhage and periventricular leukomalacia. Preterm neonates have immature immune system. The fragile co-regulation between immune defense mechanisms and immunosuppression (tolerance) is often disturbed at this category of patients. They are at high risk of sepsis due to this imbalance between the defense and suppression mechanisms but also several injuries can contribute to the onset or perpetuation of sustained inflammation. They experience altered antigen exposure in contact with hospital-specific germs, artificial devices, drugs, nutritional antigens, and hypoxia or hyperoxia. This is more significant at extremely preterm infants less than 28 weeks of gestation as they have not developed adaptation processes to tolerate maternal and self-antigens.

3

"These studies indicate that homologous blood transfusion affects the outcome of clinical diseases in both beneficial and adverse ways. Experimental situations are not suitable for randomized clinical trials - transfusions cannot be given to prevent the onset of diabetes or wound strength measured in man following receipt of homologous or autologous blood. These experimental observations indicate that the outcomes of numerous clinical diseases which have not been studied may be manipulated by the use of homologous blood or that transfusion should be avoided. Several studies indicate that changes in immune function following transfusion are permanent. The number of clinical phenomena associated with immune suppression and attributable to blood transfusion is unknown. SUMMARY Given the evidence presented here it would be foolish to suggest that transfusion of homologous blood has no immunologic consequences for the recipient. Blood transfusion is the oldest form of transplant - no one would argue that transplantation between unrelated individuals has no influience on the immune system. In organ transplantation the immunologic sequelae are permanent and there is evidence that the same is true following homologous blood transfusion. Lymphocytopenia is present one year following surgery for Crohn's disease if patients receive perioperative blood transfusion (43). Colorectal cancer patients transfused more than seven years prior to diagnosis have significantly reduced numbers of lymphocytes and lower natural killer cytotoxicity than colorectal cancer patients who have never been transfused (44). Transfusion of neonates causes suppression of lymphocyte reactivity which is still demonstrable 25 to 30 years later (45). There is evidence that transfusion at any time prior to elective surgery increases susceptibility to infectious complications (14) and otherwise healthy transfused individuals may be at increased risk of developing malignancies (46). All the longterm consequences of blood transfusion are not negative: Survival of transplants is prolonged by pretransplant transfusion and some women suffering from recurrent spontaneous abortion can deliver at term if previously transfused with their spouse's leukocytes. In the future we will be able to transfuse blood without causing immune perterbations and the consequent clinical phenomena. Studies presented here suggest that removal of donor leukocytes reduces the risk of infection and cancer recurrence. The technology has not reached the point of reducing the leukocyte number in transfused blood below 10^/unit. An alternative which is increasingly being utilized is autologous blood programs. Physicians are discovering that patients tolerate hemoglobin levels which were previously unacceptably low and many patients prefer being anemic over the risks of receiving homologous blood. Since transfusion is an identifier of high cost hospitalized patients, alternatives to routine blood use are being studied in hopes of safely reducing the costs of transfusion. REFERENCES 1. Jubert AV, Lee ET, Hersh EM, McBride CM. J Surg Res 15:399-403, 1973. 2. M 19 u4n ( s3t ) e3r4A6-M 35 , 2 W , i1n9c8h1u . rch RA, Keane RM, Shatney CH, Ernst CB, Nuidema GD. Ann Surg." In Transfusion Immunology and Medicine, 300. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-29.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.