Gotowe bibliografie tematyczne / Autoimmunity

Gotowa bibliografia na temat „Autoimmunity”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 7 lipca 2024

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Artykuły w czasopismach na temat "Autoimmunity"

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Toubi, Elias, i Zahava Vadasz. "Think autoimmunity, breath autoimmunity, and learn autoimmunity". Clinical Rheumatology 38, nr 5 (12.04.2019): 1227–30. http://dx.doi.org/10.1007/s10067-019-04540-2.

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Niederle, B. "Autoimmunität bei schilddrüsenerkrankungen—autoimmunity in thyroid disorders". European Surgery 17, nr 4 (sierpień 1985): 80. http://dx.doi.org/10.1007/bf02656416.

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Hansen, Niels. "Philosophical Approach to Neural Autoantibodies in Psychiatric Disease—Multi-Systemic Dynamic Continuum from Protective to Harmful Autoimmunity in Neuronal Systems". Antibodies 12, nr 1 (23.12.2022): 1. http://dx.doi.org/10.3390/antib12010001.

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(1) Background: philosophical views are important to enable a general and multi-systemic view of the potential understanding of autoimmunity in psychiatric disease that is not solely reflected by an immunological viewpoint. (2) Methods: we reviewed current theories of autoimmunity. (3) Results: we propose a novel area view integrating the “self/non-self” and “continuity” model into the expression of varied forms of autoimmunity in psychiatric disease, ranging from protective to harmful autoimmunity consequences framed into micro-systems (nerve cells) and macro-systems (neuronal networks), termed the “multi-systemic dynamic continuum model”. (4) Conclusions: autoimmunity’s dynamic spectrum is delineated here as something that probably functions as a whole entity to maintain, first of all, human homeostasis in behavior affecting cells or neuronal networks differently, and secondly to prevent psychiatric disease.
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Kaprara, Athina, i Gerasimos Krassas. "Thyroid autoimmunity and miscarriage". HORMONES 7, nr 4 (15.10.2008): 294–302. http://dx.doi.org/10.14310/horm.2002.1210.

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Schwarz, Marvin. "Autoimmunity". Chest 148, nr 6 (grudzień 2015): 1367–69. http://dx.doi.org/10.1378/chest.15-1323.

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Diamond, Betty. "Autoimmunity". Immunological Reviews 204, nr 1 (kwiecień 2005): 5–8. http://dx.doi.org/10.1111/j.0105-2896.2005.00258.x.

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Dalmau, Josep. "Autoimmunity". Neurology - Neuroimmunology Neuroinflammation 2, nr 6 (grudzień 2015): e181. http://dx.doi.org/10.1212/nxi.0000000000000181.

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McDuffie, Marcia, i Anthony Hayward. "Autoimmunity". Current Opinion in Pediatrics 3, nr 5 (październik 1991): 874–79. http://dx.doi.org/10.1097/00008480-199110000-00020.

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Bell, Elaine, i Lucy Bird. "Autoimmunity". Nature 435, nr 7042 (czerwiec 2005): 583. http://dx.doi.org/10.1038/435583a.

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McDevitt, HughO, i EdwardK Wakeland. "Autoimmunity". Current Opinion in Immunology 10, nr 6 (grudzień 1998): 647–48. http://dx.doi.org/10.1016/s0952-7915(98)80083-6.

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Rozprawy doktorskie na temat "Autoimmunity"

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Cucurella, Paula. "Autoimmunity in Antipoetry". Thesis, State University of New York at Buffalo, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10639684.

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Antipoetry, a form of poetry developed by the Chilean poet Nicanor Parra, instances a privileged example of a self-regulatory trait of the poetic genre which responds to poetry’s need to destroy itself in order to renew itself. This need reveals a structural mechanism or a logic of autoimmunity, which informs the possibility of language and, moreover, of all living beings.

Antipoetry’s departure from the Nerudean poetic tradition justifies the use of a colloquial language that also preserves and continues Neruda’s interest in opening a space for the “popular” in poetry. Against Neruda, Antipoetry also consciously repels romantic and heroic aesthetic principles and ideas.

Parra’s aesthetic principles, however, do not result solely from avoidance. Parra is a realist poet heavily influenced by physics. His poetry needs to mirror reality. The principles of relativity and indetermination play major roles in his poetic experimentations, and will come to the aid of Antipoetry’s need to create in times of censorship. Parra’s experiments with language are in large measure interpretations of the laws of physics. In this regard, his scientific realism is related to Gertrude Stein’s work. The poetry and poetics of the latter provides a touchstone and a constant reference in Autoimmunity in Antipoetry.

Like all artistic expressions during the Chilean military dictatorship of Augusto Pinochet, Antipoetry was forced to negotiate what could be said with what the poet wanted to say. The necessary negotiation that Parra’s poetry needed to undergo gave rise to many experiments with language, including systematic ambiguity, contestation of the authority of the author, and of his own authorial control over his poetry. The use of masks, the multiplication of referents, and the systematic use of contradiction name some of Antipoetry’s tools for obstructing the univocal determination of meaning.

Antipoetry’s systematic explorations toward the creation of a poetry that attempts to fight all forms of dogmatism nevertheless reaches a limit in its figuration of gender. Antipoetry’s gender politics makes concessions to a type of gender dogmatism (sexism and homophobia) that contradicts the antipoetic program and reveals an inherent fear of gender contamination that jeopardizes Antipoetry’s most fortunate aspects.

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Grant, Michael David. "Alloimmunity, autoimmunity, and AIDS". Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/27465.

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The sensitivity of the human immune system to the retrovirus HIV is difficult to explain on the basis of viral cytopathicity. AIDS develops often long after initial HIV infection in spite of a vigorous and sustained immune response against the virus which effectively contains viral replication. Although more virulent strains of HIV can be isolated from immunodeficient persons, there is no evidence that these strains predominate in vivo or that a large increase in production of infectious virus accompanies progression to disease. There is as yet no satisfactory mechanism to explain the immunosuppression, T4 cell depletion, autoimmunity, and immunodeficiency associated with HIV infection. An hypothesis that AIDS results from immune responses to HIV gp120 and to allogeneic cells stems from recent developments in the symmetrical network theory. It is proposed that T-cell selection processes produce a T-cell idiotypic network "centrepole," which bears an internal image of self MHC class II within T-cell receptors. This network centrepole interacts with the anti-class II helper cell repertoire to stabilize both its own expression and expression of the helper T-cell repertoire. The idiotypes involved in this mutual stabilization are related to certain idiotypes present on allogeneic lymphocytes and to the envelope glycoprotein of HIV gp120. Through its relationship to CD4 protein, and hence class II MHC, HTV gp120 is thought to mimic the T-cell network centrepole. Anti-host class II receptors on allogeneic lymphocytes induce antibodies which also mimic the proposed centrepole. The immune response to gp120 is directed against the centrepole and against the antibodies (anti-anti-class II) induced by the receptors of allogeneic lymphocytes. The hypothesis evaluated in this thesis project is that the immune responses described above synergize in an attack on both the centrepole and the helper cell repertoire, resulting in aberrant immune regulation, autoimmunity, and eventually, AIDS. Sera from persons with AIDS or at risk of AIDS were examined for antibodies implicated in the above scheme. Anti-anti-CD4/anti-gp120 antibodies (putative anti-centrepole) were found in only a small minority of subjects and did not correlate with disease, while anti-anti-class II antibodies were almost never detected. Anti-MHC class I antibodies, reflecting alloimmunity, were associated with HIV infection and to some extent with disease progression. Autoantibodies against denatured collagen, reflecting autoimmunity, were found in almost all AIDS patients. The prevalence of these autoantibodies increases in HIV infection and with disease expression. Antibodies against denatured collagen show an interesting distribution which suggests they are related to the idiotypic determinants involved in the pathogenesis of AIDS and other similar immune disorders. The specificity of these antibodies suggests they arise through immunoregulatory defects induced through idiotypic network interactions.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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Ye, Ping. "Autoimmunity in chronic periodontitis". Thesis, The University of Sydney, 2003. http://hdl.handle.net/2123/4256.

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Profound perturbation of epithelial structure is a characteristic feature of the immunopatholoical response to bacterial antigens considered to be central in the pathogenesis of the destructive lesion of periodontitis. The pathological basis for the disturbance of epithelial structure is not understood. It was demonstrated that the structural integrity and functional differentiation of the lining epithelium is compromised in relation to inflammatory changes associated with destructive periodontitis. In the pathological lining epithelium of the periodontal pocket there was a marked reduction of epithelial cadherin important in intercellular adhesion, of involucrin, a marker of terminal differentiation, and of the gap junction connexions that form intercellular communication channels. These changes were associated with alterations of filamentous actin expression, collectively indicating profound perturbation of epithelial structure. The data reported support the concept that the ability of the pathological lining epithelium to function as an effective barrier against the ingress of microbial products into the tissues is severely compromised (Ye et al., 2000). In addition, a recent study (Ye et al., 2003) by Western analysis of serum IgG from all 22 patients with chronic periodontitis tested indicated recognition of multiple epithelial components in individual patterns. In contrast, subjects with a healthy periodontium displayed only trace recognition of epithelial antigens. Levels of epithelial-reactive antibodies were significantly correlated with attachment loss as an indication of disease activity. To investigate a possible relationship between the bacterial flora adjacent to the diseased sites and the presence of epithelial-reactive antibodies, subgingival plague samples were taken from deep periodontal pockets and cultured anaerobically. Gram positive bacteria containing antigens potentially cross-reactive with epithelial cells were reproducibly isolated by probing membrane colony lifts with affinity-isolated (epitheial-specific) antibodies. The bacteria were identified as streptococci (S. mitis, S. constellatus and two S. intermedius strains) and Actinomyces (A. georgiae, and A. sp. oral clone) by 16S rDNA sequence homology. Recognition by affinity-isolated antibodies of antigens from the captured organisms was confirmed by Western analysis. Conversely, absorption of affinity-isolated antibodies with bacterial species specifically reduced subsequent recognition of epithelial antigens. To identify the auto-antigens, a human keratinocyte cDNA expression library in Lambda phage was probed using a pooled sera. Groups of responders were detected for CD24 (a recently described adhesion molecule also known as P-selectin ligand), antioxidant protein 2 (a newly recognised member of the thiol-dependment anti-oxidant proteins), lavtate dehydrogenase A, the transcription factor NFAT5, and for three genes encoding novel proteins. Six identified bacteria, especially S intermedius were demonstrated to absorb antibodies reaching with identified auto-antigens in patterns varying between individuals. This evidence indicated that during the course of periodontits, subjects develop increased levels of antibodies to common oral bacteria amongst which are included tissue cross-reactive antigens. Periodontitis could therefore present a risk for the subsequent initiation or exacerbation of a broad spectrum of disease processes including autoimmune, inflammatory, proliferative and degenerative disorders.
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Ye, Ping. "Autoimmunity in chronic periodontitis". University of Sydney, 2003. http://hdl.handle.net/2123/4256.

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Doctor of Philosophy
Profound perturbation of epithelial structure is a characteristic feature of the immunopatholoical response to bacterial antigens considered to be central in the pathogenesis of the destructive lesion of periodontitis. The pathological basis for the disturbance of epithelial structure is not understood. It was demonstrated that the structural integrity and functional differentiation of the lining epithelium is compromised in relation to inflammatory changes associated with destructive periodontitis. In the pathological lining epithelium of the periodontal pocket there was a marked reduction of epithelial cadherin important in intercellular adhesion, of involucrin, a marker of terminal differentiation, and of the gap junction connexions that form intercellular communication channels. These changes were associated with alterations of filamentous actin expression, collectively indicating profound perturbation of epithelial structure. The data reported support the concept that the ability of the pathological lining epithelium to function as an effective barrier against the ingress of microbial products into the tissues is severely compromised (Ye et al., 2000). In addition, a recent study (Ye et al., 2003) by Western analysis of serum IgG from all 22 patients with chronic periodontitis tested indicated recognition of multiple epithelial components in individual patterns. In contrast, subjects with a healthy periodontium displayed only trace recognition of epithelial antigens. Levels of epithelial-reactive antibodies were significantly correlated with attachment loss as an indication of disease activity. To investigate a possible relationship between the bacterial flora adjacent to the diseased sites and the presence of epithelial-reactive antibodies, subgingival plague samples were taken from deep periodontal pockets and cultured anaerobically. Gram positive bacteria containing antigens potentially cross-reactive with epithelial cells were reproducibly isolated by probing membrane colony lifts with affinity-isolated (epitheial-specific) antibodies. The bacteria were identified as streptococci (S. mitis, S. constellatus and two S. intermedius strains) and Actinomyces (A. georgiae, and A. sp. oral clone) by 16S rDNA sequence homology. Recognition by affinity-isolated antibodies of antigens from the captured organisms was confirmed by Western analysis. Conversely, absorption of affinity-isolated antibodies with bacterial species specifically reduced subsequent recognition of epithelial antigens. To identify the auto-antigens, a human keratinocyte cDNA expression library in Lambda phage was probed using a pooled sera. Groups of responders were detected for CD24 (a recently described adhesion molecule also known as P-selectin ligand), antioxidant protein 2 (a newly recognised member of the thiol-dependment anti-oxidant proteins), lavtate dehydrogenase A, the transcription factor NFAT5, and for three genes encoding novel proteins. Six identified bacteria, especially S intermedius were demonstrated to absorb antibodies reaching with identified auto-antigens in patterns varying between individuals. This evidence indicated that during the course of periodontits, subjects develop increased levels of antibodies to common oral bacteria amongst which are included tissue cross-reactive antigens. Periodontitis could therefore present a risk for the subsequent initiation or exacerbation of a broad spectrum of disease processes including autoimmune, inflammatory, proliferative and degenerative disorders.
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Ye, Ping. "Autoimmunity In Chronic Periodontitis". Thesis, The University of Sydney, 2003. http://hdl.handle.net/2123/4872.

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Crisi, Giovanna M. "Autoimmunity and effect of ageing". [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=8571.

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Wodzig, Karel Willem Henricus. "Cyclosporine A-induced experimental autoimmunity". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1993. http://arno.unimaas.nl/show.cgi?fid=9486.

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Johnstone, Thomas W. "Neutrophil serine proteinases and autoimmunity". Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241372.

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Bari, Abu-saleh Mahfuzul. "Autoimmunity in canine joint disease". Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257145.

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D'Cruz, David Pascal. "Autoimmunity, endothelium and vascular disease". Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298705.

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Książki na temat "Autoimmunity"

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International Conference on Autoimmunity (5th 2006 Sorrento, Italy). Autoimmunity. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2007.

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Perl, Andras. Autoimmunity. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592598056.

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Perl, Andras, red. Autoimmunity. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60761-720-4.

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Górski, Andrzej, Hubert Krotkiewski i Michał Zimecki, red. Autoimmunity. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0981-2.

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Ollier, W. Autoimmunity. Oxford: Bios Scientific Publishers, 1992.

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Pinchera, A., S. H. Ingbar, J. M. McKenzie i G. F. Fenzi, red. Thyroid Autoimmunity. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0945-1.

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Itoh, Masahiro. Testicular Autoimmunity. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-54460-9.

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Zouali, Moncef, red. Molecular Autoimmunity. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/b105867.

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E, Bigazzi Pierluigi, i Reichlin Morris, red. Systemic autoimmunity. New York: Marcel Dekker, 1991.

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1954-, Rayner David, i Champion Brian, red. Thyroid autoimmunity. Austin: R.G. Landes, 1995.

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Części książek na temat "Autoimmunity"

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Ray, Donna, i Raymond Yung. "Autoimmunity". W Nutrition in Epigenetics, 165–71. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9780470959824.ch9.

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Nahler, Gerhard. "autoimmunity". W Dictionary of Pharmaceutical Medicine, 12. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-89836-9_99.

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Dias Da Silva, Wilmar, i Dietrich Götze. "Autoimmunity". W Fundamentals of Immunology, 383–413. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70393-5_13.

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Cosentino, Marco, Natasa Kustrimovic i Franca Marino. "Autoimmunity". W Neuroimmune Pharmacology, 395–406. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44022-4_26.

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Mehlhorn, Heinz. "Autoimmunity". W Encyclopedia of Parasitology, 245. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_314.

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Mehlhorn, Heinz. "Autoimmunity". W Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-642-27769-6_314-2.

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Jeskey, Jack, Lauren Fill, Madiha Huq, Sandeep Sarkaria, Remie Saab i Robert Hostoffer. "Autoimmunity". W Absolute Allergy and Immunology Board Review, 185–91. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-12867-7_19.

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Gooch, Jan W. "Autoimmunity". W Encyclopedic Dictionary of Polymers, 876. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13201.

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Alkhatib, Ahed J. "Autoimmunity". W The Role of Microbes in Autoimmune Diseases, 29–43. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1162-0_4.

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Chauhan, Ramswaroop Singh, Yashpal Singh Malik, M. Saminathan i Bhupendra Nath Tripathi. "Autoimmunity". W Essentials of Veterinary Immunology and Immunopathology, 89–119. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-2718-0_4.

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Streszczenia konferencji na temat "Autoimmunity"

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tousheed, syed Z., vandana D. pradhan, Manisha Patwardhan, Amita U. Athavale i Kanjksha Ghosh. "Mycobacterium Tuberculosis Triggers Autoimmunity". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1393.

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Kazi, I., S. Vallejo i R. A. Estrada. "Suffocated by Autoimmunity: A Bloodbath". W American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5332.

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Bach, Jean-Francois. "SP0012 THE HYGIENE HYPOTHESIS IN AUTOIMMUNITY". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8421.

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Magalhães, Andreia, i Michiel Tent. "Tau autoimmunity associated with systemic disease". W EAN 2022 Congress, redaktorzy Andreia Magalhães i Hans-Peter Hartung. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/8aaa8090.

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Lino, Andreia. "SP0084 POST-ACTIVATED B CELLS IN AUTOIMMUNITY". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8527.

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Van Wijk, F. "SP0093 Resetting the immune system in autoimmunity". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7703.

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Beltramo, Guillaume, Nicolas Peron, Pascale Nicaise, Claire Danel, Marie-Pierre Debray, Pauline Pradère, Aurélien Justet i in. "Anti-parietal cell autoimmunity in IPF patients". W ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa779.

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Rönnblom, L. "SP0047 Type i interferon system in autoimmunity". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7134.

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Rosen, A. "SP0017 Shared mechanisms in cancer and autoimmunity". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7165.

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Felisberto, Fabíula Heinzen, Ana Paula Beckhauser, Thelma Larocca Skare, Renato Nishiara i Alessandro Tonial. "CAN BARIATRIC SURGERY HELP TO PREVENT AUTOIMMUNITY?" W XL Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2023. http://dx.doi.org/10.47660/cbr.2023.1898.

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Raporty organizacyjne na temat "Autoimmunity"

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David, Carol. Amphyphysin Autoimmunity in Breast Cancer and Stiff-Man Syndrome. Fort Belvoir, VA: Defense Technical Information Center, październik 1997. http://dx.doi.org/10.21236/ada335816.

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Cancro, Michael. Mechanisms Regulating Plasma Cell Persistence in Health and Autoimmunity. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2011. http://dx.doi.org/10.21236/ada553930.

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Baccala, Roberto. Homeostatic T Cell Expansion to Induce Anti-Tumor Autoimmunity in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2006. http://dx.doi.org/10.21236/ada456894.

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Nelson, Brad H. Eliciting Autoimmunity to Ovarian Tumors in Mice by Genetic Disruption of T Cell Tolerance Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2002. http://dx.doi.org/10.21236/ada409619.

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Gontar, I. P., O. A. Rusanova, O. I. Emelyanova, S. S. Khortieva i E. G. Cherkesova. AUTOIMMUNITY ISSUES IN PATIENTS WITH SYSTEMIC SCLERODERMA AND SYSTEMIC LUPUS ERYTHEMATOSUS WITH PREDOMINANT PULMONARY INVOLVEMENT. "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-73-81.

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Gontar, I. P., O. A. Rusanova, O. I. Emelyanova, O. V. Paramonova i E. A. Bondarenko. INFORMATIVE VALUE OF PARAMETERS OF AUTOIMMUNITY TO THYROXIN AND TRIIODOTHYRONINE IN PATIENTS WITH RHEUMATOID ARTHRITIS. "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-82-89.

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Nelson, Brad H. Eliciting Autoimmunity to Ovarian Tumors in Mice by Genetic Disruption of T Cell Tolerance Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2006. http://dx.doi.org/10.21236/ada462679.

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Kaplan, Alan M. Program in Functional Genomics of Autoimmunity and Immunology of yhe University of Kentucky and the University of Alabama. Office of Scientific and Technical Information (OSTI), październik 2012. http://dx.doi.org/10.2172/1053051.

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