Relevant bibliographies by topics / Immune pathology

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Immune pathology'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Immune pathology"

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TOMONAGA, Masao. "Immune Pathology of Myelodysplastic Syndromes." Internal Medicine 40, no. 10 (2001): 985–86. http://dx.doi.org/10.2169/internalmedicine.40.985.

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COOKE, T. D. V., and B. CHIR. "Immune Pathology in Polyarticular Osteoarthritis." Clinical Orthopaedics and Related Research &NA;, no. 213 (December 1986): 41???49. http://dx.doi.org/10.1097/00003086-198612000-00006.

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Kozakowski, N., H. Herkner, G. A. Bohmig, Z. Kikic, D. J. Cooper, K. Eller, A. H. Kirsch, et al. "PATHOLOGY: IMMUNE AND INFLAMMATORY MECHANISMS." Nephrology Dialysis Transplantation 29, suppl 3 (May 1, 2014): iii448—iii450. http://dx.doi.org/10.1093/ndt/gfu171.

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Bucelli, Robert C., and Alan Pestronk. "Immune myopathies with perimysial pathology." Neurology - Neuroimmunology Neuroinflammation 5, no. 2 (January 18, 2018): e434. http://dx.doi.org/10.1212/nxi.0000000000000434.

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ObjectiveImmune myopathies with perimysial pathology (IMPP) have a combination of damage to perimysial connective tissue and muscle fiber necrosis, more prominent near the perimysium. We studied the clinical and laboratory correlates of patients with pathologically defined IMPP.MethodsThis is a retrospective chart and pathology review of 57 consecutive patients with IMPP myopathology and, for comparison, 20 patients with dermatomyositis with vascular pathology (DM-VP).ResultsCompared with DM-VP, IMPP patients more commonly had interstitial lung disease (ILD) (p < 0.01), Raynaud phenomenon (p < 0.05), mechanic's hands (p < 0.05), arthralgias (p < 0.001), and a sustained response to immunomodulatory therapy (p < 0.05), and less frequently had a concurrent malignancy (p < 0.01). IMPP patients had higher serum creatine kinase values (p < 0.05), more frequent serum Jo-1 (p < 0.03) or SSA/SSA52 autoantibodies (p < 0.05), and less frequent antinuclear antibodies (p < 0.01). IMPP patients with serum Jo-1/antisynthetase antibodies were more likely to have ILD (p < 0.05) and inflammatory arthritis (p < 0.05) than IMPP patients without these antibodies.ConclusionsIMPP myopathology is associated with an increased risk of ILD, Raynaud phenomenon, mechanic's hands, and inflammatory arthritis when compared with another immune myopathy (DM-VP). IMPP patients require regular screening for ILD, particularly those with antisynthetase antibodies. The absence of myositis-specific autoantibodies in a large percentage of IMPP patients emphasizes the important role for myopathology in identifying patients at higher risk of severe comorbid conditions such as ILD.
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Hayes, M. M., P. Jacobs, L. Wood, and D. M. Dent. "Splenic pathology in immune thrombocytopenia." Journal of Clinical Pathology 38, no. 9 (September 1, 1985): 985–88. http://dx.doi.org/10.1136/jcp.38.9.985.

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Dienes, Hans-Peter, and Uta Drebber. "Pathology of Immune-Mediated Liver Injury." Digestive Diseases 28, no. 1 (2010): 57–62. http://dx.doi.org/10.1159/000282065.

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Racusen, Lorraine C. "Pathology and the Allo-Immune Response." American Journal of Transplantation 3, no. 12 (November 21, 2003): 1461–62. http://dx.doi.org/10.1046/j.1600-6135.2003.00288.x.

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Shmagel, K. V., and V. A. Chereshnev. "Molecular bases of immune complex pathology." Biochemistry (Moscow) 74, no. 5 (May 2009): 469–79. http://dx.doi.org/10.1134/s0006297909050010.

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Tlish, M. M., E. B. Popovskayа, N. L. Sycheva, N. V. Sorokina, and F. A. Psavok. "ASSOCIATED PATHOLOGY: CLINICAL ОBSERVATION." Vestnik dermatologii i venerologii 93, no. 4 (August 9, 2017): 66–73. http://dx.doi.org/10.25208/0042-4609-2017-93-4-66-73.

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The article analyzes the literature on polymorbidity of immune dermatoses. They confirm the possibility of combining with each other immune diseases, due to the presence of immune and metabolic abnormalities that are characteristic for the majority of chronic dermatoses and may indicate the possibility of combining several nosology. We present 2 clinical cases polymorbidity. In the first case — a combination demonstrated in one patient planus, idiopathic atrophoderma Pasini — Pierini and multi-colored lichen. In the second case detected combination of 4 kinds of dermatological diseases — horny eczema, psoriasis vulgaris, scleroderma, and rosacea. Patients underwent complex clinical examination and histomorphological examination of skin biopsies. The presented clinical cases demonstrate the possibility of a combination of several skin diseases in one patient with common etiopathogenic mechanisms
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Tousankina, I. A. "SOME ISSUES OF DIAGNOSTICS IN IMMUNE PATHOLOGY." Medical Immunology (Russia) 12, no. 6 (July 21, 2014): 485. http://dx.doi.org/10.15789/1563-0625-2010-6-485-496.

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Dissertations / Theses on the topic "Immune pathology"

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Crowley, Thomas. "Innate immune memory in fibroblasts." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8060/.

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The innate immune system is a generic response to infection or injury. Evidence shows the innate response has immunological memory capable of altering subsequent responses to stimuli. Fibroblasts are ubiquitous stromal cells capable of responding to inflammatory triggers, and of orchestrating endothelial cell and leukocyte behaviour during inflammation. Repeated challenge with cytokines (such as tumour necrosis factor (TNF) a) induced an augmented second response to stimulation. Fibroblasts from multiple anatomical locales significantly increased cytokine secretion upon second challenge with TNFa. The precise mediators augmented depended on fibroblast site of origin. Depending on site, memory was inherent, or only present in fibroblasts from chronically-inflamed tissue. This suggests a phenomenon intrinsic to some sites but pathological in others. The secreted mediators from the fibroblast initial or memory responses exerted differing effects on leukocytes, dependent upon fibroblast site of origin. Finally, examination of intracellular signalling showed the augmented response was at least partly due to prolonged activity of nuclear factor (NF) KB during the memory response. Innate immune memory exists in fibroblasts from multiple tissues, but may be pathologically acquired in some. The altered response to second challenge may represent a fibroblast mechanism for altering the recruitment and behaviour of the inflammatory infiltrate.
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McIntosh, Alistair James. "The role of adipose tissue immune cells in immune responses." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8113/.

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Recent evidence indicates that immune cells within adipose tissues can drive the formation of ectopic lymphoid structures, known as Fat Associated Lymphoid Clusters (FALC). FALC support B-cell antibody production in response to infection and inflammation. This investigation explores the immune cell composition and role of different adipose tissues both in steady state and during immune responses in mice. Firstly, a detailed analysis of the immune cell composition of peritoneal adipose tissues was performed. To investigate the function and migratory properties of these tissue-resident cells, cytokine and chemokine receptor expression was then assessed. How immune cells in adipose tissues responded to infection was examined using an intestinal helminth infection with the parasite Heligmosomoides polygyrus. Adipose tissues predominantly contained regulatory T cells, invariant natural killer T cells and group 2 Innate Lymphoid Cells (ILC2s). Significant differences were observed in composition, cell surface markers and cytokine production of ILC2s between adipose depots and secondary lymphoid tissues, indicating that tissue specific signals can direct ILC2 responses. Finally, increases were observed in ILC2 and FALC numbers in the mesenteries of WT mice following parasite infection. These data indicate that immune cells within adipose tissues respond to infection and may contribute to immune responses.
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Oswald, Douglas Martin. "LOCAL AND SYSTEMIC IMMUNE REGULATION BY LIVER AND PLASMA PROTEIN GLYCOSYLATION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1575642172980456.

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Read, Simon. "The role of CD4'+' regulatory T cells in protection from inflammatory bowel disease : phenotype, ontogeny and mechanism of action." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365754.

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Pang, Terence Tat Lun. "Adiponectin and immune tolerance in type 1 diabetes." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1762/.

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Type 1 diabetes (T1D) is characterised by pancreatic cell autoimmunity and inflammation, resulting in cell islet destruction and insulin deficiency. Prospective studies from different continents have shown that insulin resistance is independently associated with risk for the development of T1D. We wanted to investigate the role of adiponectin in mediating this link. Adiponectin is a circulating adipokine whose anti-inflammatory and insulin sensitising actions appear to be mediated via two related receptors, AdipoR1 and AdipoR2. We began by characterising adiponectin receptor expression on PBMC by flow cytometry. We showed that monocytes express both receptors abundantly, that this expression correlates with insulin sensitivity in both health and diabetes. Furthermore, expression can be increased with lifestyle intervention. Adiponectin receptor expression on monocytes is reduced in T1D, and we demonstrate this leads to an apparent resistance in the ability of adiponectin to inhibit the stimulatory capacity of antigen presenting cells (APC). Specifically, we show that adiponectin inhibits the stimulatory capacity of APCs through down-regulation of CD86 expression, and that this effect is decreased in T1D. In this way, the release from the regulatory effects of adiponectin is one potential mechanism by which immune tolerance is lost in T1D.
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Malik, Suneil. "Genetics of host innate immune factors in Tuberculosis susceptibility." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85578.

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Tuberculosis, caused by Mycobacterium tuberculosis, is globally a leading cause of morbidity and mortality. While a host genetic contribution to tuberculosis susceptibility is known to occur, the extent and nature of host genetic variability to tuberculosis pathogenesis are unknown. Thus, to better understand the role of host genetic factors in tuberculosis susceptibility, we have tested the contribution of candidate gene variants to tuberculosis susceptibility in three geographically, epidemically, and clinically distinct populations. We chose four candidate genes involved in the innate immune response, namely, NRAMP1, MBL, SFTPA1, and SFTPA2.
Since the global spread of tuberculosis is highly dependent on HIV/AIDS pandemic, we investigated the association of genetic MBL variants and HIV-1 infection in 278 Colombian HIV-infected and control individuals. MBL genotype frequencies were similar for both groups, and no association was detected between MBL alleles B, C, and D and susceptibility to HIV-1 infection (P = 1.0). These results do not support the hypothesis that MBL levels are a risk factor for HIV-1 infection in Colombia. Moreover, we were able to show that MBL variants do not contribute to tuberculosis susceptibility in this population.
In a pediatric population composed of 184 families we found allelic variants in the NRAMP1 gene to be associated with tuberculosis disease (P = 0.01; Odds ratio [OR] = 1.75 [95% confidence interval: 1.10--2.77]). Common NRAMP1 alleles were identified as risk factors for pediatric tuberculosis while these same alleles were reported to be protective in adult cases, suggesting that the common alleles promote rapid progression from infection to tuberculosis disease. Furthermore, the association of NRAMP1 with pediatric tuberculosis disease was significantly heterogeneous (P = 0.01) between simplex (P < 0.0008; OR = 3.13 [1.54--6.25]) and multiplex families (P = 1) suggesting an interplay between mechanisms of genetic control and exposure intensities. Finally, we tested the correlation between the NRAMP1 risk and NRAMP1 functional activity by measuring the recruitment efficiency of mannose-6-phosphate receptor (M6PR) to Salmonella containing vacuoles (SCV) in monocyte-derived-macrophages (MDM). We show that recruitment of M6PR to SCV is significantly lower ( P = 0.024) in MDM from patients homozygous for the risk allele as compared to MDM from heterozygous patients. Thus, altered function of NRAMP1 appears to modulate the rate of progression from infection to disease.
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Faingold, Dana. "Immune expression and inhibition of heat shock protein 90 in uveal melanoma." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=92320.

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Uveal melanoma (UM) is the most common intraocular tumor in adults. Despite the increase in diagnostic accuracy over the past several decades and the development of eye saving treatments such as plaque radiotherapy and photon beam therapy, there was no significant change in the prognosis in uveal melanoma due to metastatic disease. Therefore, we started to search for novel therapeutic targets in UM, such as heat shock protein 90 (Hsp90). This protein is a chaperone for several proteins (clients) involved in signal transduction and cell cycle control like kinases and transcription factors and plays a key role in regulating their stability and function. Hsp90 is expressed by a variety of tumor types and its inhibition results in the down regulation and proteasomal degradation of its client proteins.
The objective of this study was to examine the immunohistochemical profile of Hsp90 and its association with prognostic features in uveal melanoma. In addition, we studied the role of Hsp90 in promoting growth and survival of uveal melanoma and the molecular consequences of inhibiting Hsp90 function by the small-molecule 17-allylamino-17-demethoxy-geldanamycin (17-AAG).
Hsp90 expression was studied in five primary human uveal melanoma cell lines by Western blot analysis and immunofluorescence methods in 44 specimens of human UM, 14 specimens from an animal model of UM and also in metastatic specimens.
In addition we determined the cytotoxicity profile of five primary UM cell lines and one metastatic derived cell line (OMM-1.5) after exposure to Hsp90 inhibitor 17-AAG. Sulfurhodamine-B based proliferation assay was used to compare UM cell growth with a range of concentrations of 17-AAG. Changes in cell migration and invasion and apoptosis and cell cycle assays were evaluated by flow cytometry. The expression of intracellular proteins was determined using Western blot analysis.
Hsp90 was identified in 68 % of cases of primary uveal melanoma and was expressed in 87% of metastatic specimens. The expression of the Hsp90 in primary tumor was significantly associated with largest tumor dimension.
Inhibition of Hsp90 function by 17-AAG caused a dose-dependent growth inhibition of primary and metastatic UM cell lines. 17-AAG induced cytostasis which was associated with a decrease in cyclin-dependent kinase CDK4. Also, 17-AAG induced apoptosis with a significant increase in caspase 3-protease activity after drug exposure. The cytotoxic effect of 17-AAG was associated with decreased levels of Akt and phospho-Akt after 24 h exposure to the drug. 17-AAG significantly reduced the migratory and invasive capabilities of all 5 uveal melanoma cell lines. 17-AAG down regulated c-Met and IGF-1R receptor transmembrane tyrosine kinases and also inhibited activation of focal adhesion kinase (FAK).
For the first time in UM, we demonstrate that over expression of Hsp90 in patients is linked to an indicator of poor prognosis. To the best of our knowledge, this is the first report showing the effect of Hsp90 inhibitor 17-AAG, on proliferation of UM cells which induced cell cycle arrest and apoptosis. Downregulation of p-Akt in response to Hsp90 inhibition could represent one possible mechanism of mod-ulation of the phosphatidylinositol 3'-kinase (PI3K)-Akt pathway in uveal melanoma. Also, we demonstrated for the first time that inhibition of Hsp90 function had an effect on UM cells motility and invasive potential and in cellular processes involved in metastasis in uveal melanoma. This data indicates that UM is a suitable target for modulation of Hsp90 activity and that Hsp90 inhibitors are possible therapeutic modalities for UM patients. Prospective studies are needed to confirm the prognostic role of Hsp90 in UM and further trials in uveal melanoma models should be undertaken to study the effect of inhibition of Hsp90 in vivo.
Le mélanome uvéal (UM) est la tumeur intraoculaire primitive la plus fréquente chez les adultes. Par conséquent, nous avons commencé à la recherche de nouvelles cibles thérapeutiques dans l'UM, tels que les protéines de choc thermique 90 (Hsp90). Hsp90 est une protéine chaperon indispensable à l'activation et la régulation d'un ensemble important de protéines de la signalisation et de la régulation cellulaire. L'utilisation d'inhibiteur spécifique de Hsp90 entraîne une baisse de l'activité des protéines clientes.
L'objectif de cette étude était d'examiner le profil des Hsp90 et son association avec les caractéristiques pronostiques dans mélanome de l'uvée. En outre, nous avons étudié le rôle qu'elle joue dans les mécanismes cellulaires de prolifération de mélanome de l'uvée et les conséquences de l'inhibition de la fonction de Hsp90 par 17-allylamino-17-demethoxy-geldanamycin (17-AAG).
L'expression immunohistochimique des Hsp90 a été étudiée dans cinq lignées de cellules tumorales in-vitro par Western blot et méthodes d'immunofluorescence. L'expression de Hsp90 a été évaluée dans 44 spécimens l'UM humaine et 14 spécimens d'un modèle animal de l'UM et dans des spécimens provenant de lésions métastatiques humaines et animales. En outre, notre étude a visé à comparer les effets antiprolifératifs du 17-AAG sur les lignées cellulaire cancéreuse d'UM humaine et dans une lignée de cellules tumorales dérivées d'une lésion métastatique (OMM-1,5). La prolifération cellulaire a été évaluée par le test à la sulforhodamine B sur les cellules exposées à une gamme de concentrations de 17-AAG.
Les changements dans la migration et l'invasion cellulaire en présence ou l'absence de la 17-AAG. Le processus apoptotique et les fractions de cycle cellulaire ont été déterminés par cytométrie en flux. Analyse de l'expression de Hsp90 et l'expression de protéines intracellulaires a été déterminée par l'analyse Western blot.
L'expression des Hsp90 a été identifiée dans 68% des spécimens et a été exprimée dans 87 % des spécimens métastatique. L'expression de l'Hsp90 dans la tumeur primaire a été significativement associée à la plus grande dimension de la tumeur.
L'inhibition de la fonction Hsp90 par 17-AAG a entraîné une inhibition de croissance dose-dépendante avec une réduction statistiquement significative. 17-AAG induit arrêt du cycle cellulaire qui a été associée à une diminution de la kinase CDK4. En outre, 17-AAG induisent l'apoptose dans les cellules d'UM et une augmentation de l'activité de la caspase-3. L'effet cytotoxique de la 17-AAG a été associé à une baisse des niveaux d'Akt et phospho-Akt, 24 h après l'exposition à la drogue.
L'exposition à la 17-AAG a considérablement réduit les capacités migratoires et invasives des les cinq lignées de cellules d'UM et provoquent une baisse des niveaux de récepteurs tyrosine kinases transmembranaires c-Met et IGF-1R et aussi a également réduit l'expression de la kinase d'adhérence focale (FAK).
Pour la première fois en UM nous démontrer que l'expression de Hsp90 chez des patients est liée à un indicateur de pronostic défavorable. Nos résultats apportent des informations originales sur les effets cytotoxiques de 17-AAG sur la prolifération des cellules d'UM qui induit un arrêt du cycle cellulaire et l'apoptose. Le diminution de p-Akt en réponse à Hsp90 inhibition pourrait constituer un mécanisme possible de la modulation de la phosphatidylinositol 3'-kinase (PI3K) - Akt signalisation de mélanome de l'uvée.
L'expression de Hsp90 dans métastases et l'évaluation des processus cellulaires impliqués dans l'invasion après l'inhibition de la fonction de Hsp90 suggéré l'utilité des inhibiteurs de Hsp90 dans la prévention de la progression tumorale et les métastases. L'ensemble de nos résultats montre que le ciblage Hsp90 mai constituer une nouvelle approche thérapeutique pour les patients avec le mélanome de l'uvée.
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Nyakundi, Jane Nyamoita. "A study of intestinal pathology and its significance in Trypanosoma brucei brucei infection." Thesis, University of Salford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366023.

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Adams, Rozanne Charlene McChary. "Ontogeny of the innate immune response in healthy South African infants." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/71834.

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Thesis (MScMedSc)--Stellenbosch University, 2012.
Includes bibliography
ENGLISH ABSTRACT: Infection is a major cause of morbidity and mortality in infants within the first few months of life. Susceptibility to infectious disease in this vulnerable population is more prevalent in resource-limited regions, with a higher disease burden. Due to certain deficiencies in their adaptive immune system, neonates rely predominantly on their innate immune system for protection against infection, a vital component in the early host defence against pathogens. Several studies have described differences in neonatal innate toll-like receptor-mediated responses compared to adult counterparts, though very little is known about these receptor responses within resource-limited settings. To address this issue, we assessed the longitudinal development of cytokine-specific responses of TLR4 and TLR7/8 in monocytes, myeloid dendritic cells and plasmacytoid dendritic cells in infants from a resource-limited setting, South Africa, within the first 12 months of life and compared it to adults. Contrary to previously published literature, we observed heightened production of TH-1 cytokines: we showed increased responsiveness to TLR4 and TLR7/8 stimulation in infants at two and six weeks of age, which may be due to vaccination administered at birth. Unexpectedly, the hyper-inflammatory response persisted at six months in response to the LPS (TLR4) stimulus. This increased response at six months may be attributed to decreased passive immunity through infant weaning as well as increased exposure to microbial pathogens in this setting. Maturation of most cytokine responses was reached at twelve months for the TLR4 receptor, and at six months for the TLR7/8 receptor. The first year of life represents a critical period for maturation of the immune response. Data from this study point towards an elevated response within the first six months of life. This heightened response reflects both an ability to mount a sufficient TH-1 response in infancy, but more likely, the increased exposure to microbial stimuli in the environment. Thus, we speculate that these age-specific inflammatory responses may influence the outcome of immune responses to various vaccines administered, which may result in altered responsiveness to immunisation in infancy.
AFRIKAANSE OPSOMMING: Die hoof oorsaak vir morbiditeit en mortaliteit in babas binne die eerste paar maande van hul lewe word toegeskryf aan infeksie. In hulpbron beperkte gebiede, gekenmerk deur `n groter siektelas, is daar `n verhoogde vatbaarheid vir infeksie in hierdie kwesbare populasie. As gevolg van sekere gebreke in die verworwe immuunstelsel, maak pasgebore babas hoofsaaklik staat op hul aangebore immuunstelsel vir beskerming teen infeksie, ’n belangrike komponent vir die vroeë verdediging teen patogene. Verskeie studies het al die verskille in toll-tipe reseptor (TTR) bemiddelde reaksies tussen pasgebore babas en volwassenes vergelyk, maar nie veel is bekend oor hierdie reaksies in areas waar hulpbronne beperk is nie. Om hierdie kwessie aan te spreek is die longitudinale ontwikkeling van sitokien-spesifieke reaksies van die TTR4 en TTR7/8 reseptore van monosiete, miëloïede en plasmasitoïede dendritiese selle van babas in die hulpborn beperkte land Suid-Afrika, oor die eerste 12 maande geëvalueer en dit vergelyk met volwassenes. In teenstelling met vorige literatuur, het hierdie studie ’n polarisasie tot TH-1-sitokien produksie gevind: verhoogde reaktiwiteit van die TTR4 en TTR7/8 is gevind in babas van twee en ses weke oud, wat gedeeltelik as gevolg van die inenting kan wees wat toegedien was na geboorte. Hierdie hiper-inflammatoriese reaksie teen die TTR4 stimulus (Lipopolisakkaried (LPS), het teen verwagting voortgeduur tot op ses maande en kan toegeskryf word aan die vermindering van passiewe immuniteit deur spening, sowel as die toenemende blootstelling aan mikrobiese patogene in die omgewing. Maturasie vir die meerderheid van die sitokiene reaksies, is bereik op 12 maande vir TTR4, en op ses maande vir TTR7/8. Die eerste lewensjaar is ‘n kritiese periode vir die ontwikkeling van die immuunstelsel. Data van hierdie studie dui op ‘n verhoogde reaksie binne die eerste ses maande van ‘n baba se lewe. Hierdie verhoogde reaksie dui op die vermoë om `n voldoende TH-1 reaksie te ontlok, maar meer waarskynlik, verhoogde blootstelling aan mikrobiese stimuli in die omgewing. Dus spekuleer ons dat hierdie ouderdom-spesifieke reaksies dalk die uitkoms van die immuunreaksie teen verskeie entstof toediening kan beïnvloed in babas.
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Singh, Rekha. "Cellular immune responses in HSV and CMV infections." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/29036.

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The herpes simplex virus (HSV) and cytomegalovirus (CMV) are the prominent members of the Herpesviridae family collectively responsible for the majority of herpes-related morbidity and mortality in humans. These viruses are therefore the subjects of this study that was undertaken to improve our understanding of the nature of immune response and the mechanism of viral modulation leading to suppression of viral replication or evasion of the host immune response in vivo. The present study has examined the T helper responses to HSV-2 and murine CMV (MCMV) and provides new insights into the nature and the modulation of the T helper responses by these viruses in vivo. B7-1/B7-2 costimulation of T cells by antigen-presenting cells is essential for T cell activation by antigen. HSV-2 infection affects the expression of both B7-1 and B7-2 on monocytes, the key antigen presenting cells in vivo, potentially in two ways with opposing outcomes. It abrogates or diminishes the IFN-gamma-upregulation of B7-1 (in 8 out of 9 patients) and B7-2 (in 6 out of 9 patients) on monocytes. However, the infection also augments the expression of B7-1 and B7-2 on monocytes through an IFN-gamma-independent mechanism (in 9 out of 9 patients). Although the clinical significance of these opposing effects is presently unclear, these may be related to the immunological mechanism or strategy leading to recurrent disease in immunocompetent hosts. Like HSV-2, infections with MCMV in mice also led to a predominant Thl type immune response characterized by high levels of IFN-gamma and low IL-4 production. Studies with specific MCMV mutants, containing Tn3 transposon in the open reading frame of M25, M27, M43, or m09 gene, led to the identification of M43 gene that specifically suppresses IL-4 response. The Tn3 disruption of M43, but not M25, M27 or m09, gene of MCMV led to a strong IL-4 response (p = 0.0002) despite the presence of a dominant IFN-gamma response. These results provide insight into the possible role of a herpesvirus gene that can profoundly modulate the nature of T helper response in vivo. The presence of a homologous genetic element in other herpesvirus genomes may explain the dominant Th1 immune response triggered by HSV-2 and possibly other herpesviruses. The obvious importance of this finding, beyond herpesvirus immunopathogenesis, lies in the ability of M43 and homologous genes to globally modulate the nature of cytokine response in vivo and suppress Th2 cytokine-mediated diseases. (Abstract shortened by UMI.)
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Books on the topic "Immune pathology"

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Walker, Pam. The immune system. San Diego, Calif: Lucent Books, 2003.

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Walker, Pam. The immune system. San Diego, Calif: Lucent Books, 2003.

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Brown, Earl. Basic concepts in pathology: A student's survival guide. New York: McGraw-Hill, Health Professions Division, 1998.

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Siegfried, Ansorge, and Langner Jürgen, eds. Cellular peptidases in immune functions and diseases. New York: Plenum Press, 1997.

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Olsen, Olger M. Zufall und/oder Determination: Das Phänomen acquired immune deficiency syndrome. Osnabrück: Literarisches Büro, 1985.

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Pathology of AIDS: Textbook and atlas of diseases associated with acquired immune deficiency syndrome. Philadelphia: Lippincott, 1989.

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A, Roth James, ed. Understanding immunology. St. Louis: Mosby, 1998.

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General pathobiology. Norwalk, Conn: Appleton & Lange, 1994.

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Birch, Kate. The solution: Homeoprophylaxis, the vaccine alternative : a parent's guide to educating your child's immune system. Bloomington, IN: Balboa Press, 2012.

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Evans, Sarah Frances. A study of the immune system and some aspects of the pathology of the osteopetrotic (op/op)rat. Birmingham: University of Birmingham, 1987.

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Book chapters on the topic "Immune pathology"

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Gupta, Pallav, and Ramesh K. Gupta. "Pauci-immune Crescentic Glomerulonephritis." In Pathology of Glomerular Diseases, 161–73. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1430-0_13.

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Amaratunga, Chanaki, Tatiana M. Lopera-Mesa, Jeanette G. Tse, Neida K. Mita-Mendoza, and Rick M. Fairhurst. "Pathology and Pathogenesis of Malaria." In The Immune Response to Infection, 361–81. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch29.

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Kohli, Vinay Kumar, Chitra Kohli, and Akanksha Singh. "Immune System Disorders." In Comprehensive Multiple-Choice Questions in Pathology, 17–21. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08767-7_3.

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Pittaluga, Stefania. "Lymphoproliferative Disorders in Primary Immune Deficiencies." In Encyclopedia of Pathology, 324–34. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-95309-0_4771.

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Nagura, H., and Y. Sumi. "Secretory IgA and Mucosal Immune Responses." In Digestive Disease Pathology, 185–205. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-662-11562-6_9.

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Pittaluga, Stefania. "Lymphoproliferative Disorders in Primary Immune Deficiencies." In Encyclopedia of Pathology, 1–11. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-28845-1_4771-1.

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Britton, Warwick J., and Bernadette M. Saunders. "Pathology and Pathogenesis of Bacterial Infections." In The Immune Response to Infection, 325–36. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch26.

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Jones, Carmen Baca, and Matthias von Herrath. "Pathology and Pathogenesis of Virus Infections." In The Immune Response to Infection, 383–89. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch30.

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Wainberg, M. A., and M. S. Halpern. "Avian Sarcomas: Immune Responsiveness and Pathology." In Developments in Veterinary Virology, 131–52. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2059-3_7.

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Asa, Sylvia L., and Kalman Kovacs. "Endocrine-Immune Interactions in Pituitary Pathology." In Advances in Psychoneuroimmunology, 243–52. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9104-4_20.

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Conference papers on the topic "Immune pathology"

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Xuanwu Zhou. "Research on immune pathology in artificial immune system." In 2009 Chinese Control and Decision Conference (CCDC). IEEE, 2009. http://dx.doi.org/10.1109/ccdc.2009.5192603.

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Durkee, Madeleine S., Adam Sibley, Junting Ai, Rebecca Abraham, Vladimir M. Liarski, Marcus R. Clark, and Maryellen L. Giger. "Improved instance segmentation of immune cells in human lupus nephritis biopsies with Mask R-CNN." In Digital Pathology, edited by John E. Tomaszewski and Aaron D. Ward. SPIE, 2020. http://dx.doi.org/10.1117/12.2549751.

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Ding, Ruiwen, Prateek Prasanna, Germán Corredor, Cheng Lu, Priya Velu, Khoi Le, Patrick Leo, et al. "Compactness measures of tumor infiltrating lymphocytes in lung adenocarcinoma are associated with overall patient survival and immune scores." In Digital Pathology, edited by John E. Tomaszewski and Aaron D. Ward. SPIE, 2020. http://dx.doi.org/10.1117/12.2549588.

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Abraham, Rebecca, Madeleine S. Durkee, Margaret Veselits, Junting Ai, Jordan D. Fuhrman, Marcus R. Clark, and Maryellen L. Giger. "Application and generalizability of U-Net segmentation of immune cells in inflamed tissue." In Digital and Computational Pathology, edited by John E. Tomaszewski and Aaron D. Ward. SPIE, 2021. http://dx.doi.org/10.1117/12.2581063.

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Durkee, Madeleine S., Rebecca Abraham, Junting Ai, Marcus R. Clark, and Maryellen L. Giger. "Managing class imbalance of immune cell populations in multi-class instance segmentation of immunofluorescence images of Lupus Nephritis biopsies." In Digital and Computational Pathology, edited by John E. Tomaszewski and Aaron D. Ward. SPIE, 2021. http://dx.doi.org/10.1117/12.2581060.

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Lindhout, Ivan, and Andis Klegeris. "Neurotrophins as intercellular signaling molecules of the brain regulate select immune functions of microglia." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08927.

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Dudek, Michael, Percy Knolle, Dominik Pfister, Mathias Heikenwälder, Sainitin Donakonda, Melanie Laschinger, Daniel Hartmann, et al. "Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740803.

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Roose, Jeroen. "196 Immune pathology caused by intrinsic loss of control in CD4 T cells." In 13th International Congress on Systemic Lupus Erythematosus (LUPUS 2019), San Francisco, California, USA, April 5–8, 2019, Abstract Presentations. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-lsm.196.

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Buslaev, V. Yu, A. V. Torgunakova, Irina Milentyeva, Lyubov Dyshlyuk, and V. I. Minina. "POPYMORPHISM OF IMMUNE RESPONSE GENES AND LUNG CANCER RISK IN NON-SMOKING RESIDENTS OF KUZBASS." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-17.

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Abstract:
Lung cancer (LC) is leading oncological pathology, posing a serious threat for patient’s lives. Accordingly to World Health Organization (WHO) 2,1 million of new cases and 1,8 of deaths are annually registered. It was accumulated a lot of information about significant influence of smoking on increased risk of LC development. 80-90% of patients with LC are namely smokers. However at present time it was registered increased level of mortality from this pathology among non-smoking patients [1]. LC formation in non-smoking individuals can occur due to environmental pollution by industrial and household cancerogens and also because of molecular and genetical and cytogenetical dissimilarities. Since LC development can be associated with anomalous immunological response, immune genes can be considered as potential biological markers [2]. Objective: To assess the influence of polymorphic variants of innate immunity genes on LC development in non-smoking patients.
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Surette, M., M. Tillman, A. Mayavannan, and J. Wang. "O10.5 Repeated, low dose Chlamydia infections trigger aberrant immune responses and enhanced tissue pathology." In Abstracts for the STI & HIV World Congress, July 14–17 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/sextrans-2021-sti.108.

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Reports on the topic "Immune pathology"

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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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