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University of Manchester

1. Bagabir, Rania. Immune profiling of keloid disease.

Degree: PhD, 2013, University of Manchester

Keloid disease (KD) is a benign fibroproliferative dermal disease of unknown aetiopathogenesis that occurs in genetically susceptible individuals. KD shows high heterogeneity within the lesion, harbouring different immune cell profiles, which are poorly characterised in KD at different lesional sites. Although, it has long been appreciated that chronic inflammation and dermal fibrosis is associated with other fibrotic diseases (e.g. scleroderma), this link has not, yet, been established in KD through direct evidence. Additionally, the limited availability of a simple KD animal model has hindered our understanding of the underlying pathogenesis of KD. Therefore, the main objectives were a) to identify and profile different immune cells at defined KD lesional and histological sites, b) to further characterize the potential contribution of viral particles in KD by investigating the gene and protein expression profile of toll like receptors that recognise viral particles in KD, and c) to develop an optimized long-term serum-free organ culture (OC) model for KD research as a tool for probing novel hypotheses in KD pathobiology deduced from a) and b) and to also validate the reliability and instructiveness of this novel ex vivo KD model with conventional (e.g. dexamethasone) and potential future anti-KD compounds [(-)-epigallocatechin-3-gallate (EGCG) and plasminogen activator inhibitor-1 (PAI-1) knock-down by siRNA]. To achieve above objectives, different cellular and molecular techniques were applied. Immune profiling of KD (chapter 2) at defined lesional and histological sites generated the first comprehensive analysis of KD-associated inflammatory cell infiltrates. This work demonstrated for the first time the presence of specific type of chronic inflammation in KD that resembles the formation of tertiary lymphoid tissues (TLTs) (in 14.7%, out of 68 KD cases). Although, these TLTs are not strictly linked to defined lesional sites within the KD, they are similar in structure to mucosa-associated lymphoid tissue (MALT). Therefore, we named this phenomenon as keloid-associated lymphoid tissue (KALT). Immunophenotyping of KD lesional sites also showed a predominance of T-cells, B-cells, M2 macrophages and OX40L+ degranulated mast cells in intralesional and perilesional sites of KD compared to normal skin and normal scar tissue. In the epidermis, Langerhans cells showed no changes, whereas the intra-epidermal T-cells were significantly increased in both the intralesional and perilesional sites of KD with an increased CD4:CD8 ratio. Intra-epidermal B-cells were only rarely found in KD. Interestingly, there was no significant statistical difference between intralesional and perilesional sites of KD immunophenotyping. These abnormal immune profiles suggest the persistence of non-resolving inflammation presence towards unknown stimuli, which require further investigation. The chronic inflammation could be followed by a reparative phase in a repetitive manner leading to KD formation. Evaluation of toll-like receptor (TLR) gene…

Subjects/Keywords: 616.5; Chronic inflammation; Keloid-associated lymphoid tissue (KALT); mast cells; alternative macrophages; T-cells; B-cells; OX40L; TLR-6; TLR-7; TLR-8; keloid ex vivo organ culture; EGCG; dexamethasone and PAI-1 knockdown.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Bagabir, R. (2013). Immune profiling of keloid disease. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/immune-profiling-of-keloid-disease(49deda37-3dcf-49b4-9be6-3dc8d45f3d1d).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.570267

Chicago Manual of Style (16th Edition):

Bagabir, Rania. “Immune profiling of keloid disease.” 2013. Doctoral Dissertation, University of Manchester. Accessed September 27, 2020. https://www.research.manchester.ac.uk/portal/en/theses/immune-profiling-of-keloid-disease(49deda37-3dcf-49b4-9be6-3dc8d45f3d1d).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.570267.

MLA Handbook (7th Edition):

Bagabir, Rania. “Immune profiling of keloid disease.” 2013. Web. 27 Sep 2020.

Vancouver:

Bagabir R. Immune profiling of keloid disease. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2020 Sep 27]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/immune-profiling-of-keloid-disease(49deda37-3dcf-49b4-9be6-3dc8d45f3d1d).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.570267.

Council of Science Editors:

Bagabir R. Immune profiling of keloid disease. [Doctoral Dissertation]. University of Manchester; 2013. Available from: https://www.research.manchester.ac.uk/portal/en/theses/immune-profiling-of-keloid-disease(49deda37-3dcf-49b4-9be6-3dc8d45f3d1d).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.570267

2. Bagabir, Rania. Immune profiling of keloid disease.

Degree: 2013, University of Manchester

AbstractKeloid disease (KD) is a benign fibroproliferative dermal disease of unknown aetiopathogenesis that occurs in genetically susceptible individuals. KD shows high heterogeneity within the lesion, harbouring different immune cell profiles, which are poorly characterised in KD at different lesional sites. Although, it has long been appreciated that chronic inflammation and dermal fibrosis is associated with other fibrotic diseases (e.g. scleroderma), this link has not, yet, been established in KD through direct evidence. Additionally, the limited availability of a simple KD animal model has hindered our understanding of the underlying pathogenesis of KD. Therefore, the main objectives were a) to identify and profile different immune cells at defined KD lesional and histological sites, b) to further characterize the potential contribution of viral particles in KD by investigating the gene and protein expression profile of toll like receptors that recognise viral particles in KD, and c) to develop an optimized long-term serum-free organ culture (OC) model for KD research as a tool for probing novel hypotheses in KD pathobiology deduced from a) and b) and to also validate the reliability and instructiveness of this novel ex vivo KD model with conventional (e.g. dexamethasone) and potential future anti-KD compounds [(-)-epigallocatechin-3-gallate (EGCG) and plasminogen activator inhibitor-1 (PAI-1) knock-down by siRNA]. To achieve above objectives, different cellular and molecular techniques were applied. Immune profiling of KD (chapter 2) at defined lesional and histological sites generated the first comprehensive analysis of KD-associated inflammatory cell infiltrates. This work demonstrated for the first time the presence of specific type of chronic inflammation in KD that resembles the formation of tertiary lymphoid tissues (TLTs) (in 14.7%, out of 68 KD cases). Although, these TLTs are not strictly linked to defined lesional sites within the KD, they are similar in structure to mucosa-associated lymphoid tissue (MALT). Therefore, we named this phenomenon as keloid-associated lymphoid tissue (KALT). Immunophenotyping of KD lesional sites also showed a predominance of T-cells, B-cells, M2 macrophages and OX40L+ degranulated mast cells in intralesional and perilesional sites of KD compared to normal skin and normal scar tissue. In the epidermis, Langerhans cells showed no changes, whereas the intra-epidermal T-cells were significantly increased in both the intralesional and perilesional sites of KD with an increased CD4:CD8 ratio. Intra-epidermal B-cells were only rarely found in KD. Interestingly, there was no significant statistical difference between intralesional and perilesional sites of KD immunophenotyping. These abnormal immune profiles suggest the persistence of non-resolving inflammation presence towards unknown stimuli, which require further investigation. The chronic inflammation could be followed by a reparative phase in a repetitive manner leading to KD formation. Evaluation of toll-like receptor… Advisors/Committee Members: PAUS, RALF R, Bayat, Ardeshir, Paus, Ralf.

Subjects/Keywords: Chronic inflammation; Keloid-associated lymphoid tissue (KALT); mast cells; alternative macrophages; T-cells; B-cells; OX40L; TLR-6; TLR-7; TLR-8; keloid ex vivo organ culture; EGCG; dexamethasone and PAI-1 knockdown.

…114 Table S4: Demographic data of keloid cases with KALT… …associated lymphoid tissue (KALT). Immunophenotyping of KD lesional sites also showed a… 

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Bagabir, R. (2013). Immune profiling of keloid disease. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:189914

Chicago Manual of Style (16th Edition):

Bagabir, Rania. “Immune profiling of keloid disease.” 2013. Doctoral Dissertation, University of Manchester. Accessed September 27, 2020. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:189914.

MLA Handbook (7th Edition):

Bagabir, Rania. “Immune profiling of keloid disease.” 2013. Web. 27 Sep 2020.

Vancouver:

Bagabir R. Immune profiling of keloid disease. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2020 Sep 27]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:189914.

Council of Science Editors:

Bagabir R. Immune profiling of keloid disease. [Doctoral Dissertation]. University of Manchester; 2013. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:189914

.