P. G. Cetinkaya, D. Ayvaz, Hacer Cüzdanci, I. Tezcan
{"title":"The Association Between Vitamin D Levels and Infections in Patients with Primary Immunodeficiency","authors":"P. G. Cetinkaya, D. Ayvaz, Hacer Cüzdanci, I. Tezcan","doi":"10.25002/tji.2019.1005","DOIUrl":"https://doi.org/10.25002/tji.2019.1005","url":null,"abstract":"","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81348872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Review on Computational Tools and Databases for the Development of Vaccines Against Infectious Diseases","authors":"Q. M. S. Jamal","doi":"10.25002/tji.2019.1182","DOIUrl":"https://doi.org/10.25002/tji.2019.1182","url":null,"abstract":"","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88571962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: The up-regulation of interleukin-17 (IL-17) has been reported to be the pathogenesis of type 1 diabetes mellitus (T1D). On the other hand, vitamin D deficiency is fairly prevalent in T1D. This study aims to investigate IL-17 and vitamin D status and its correlation in children and adolescents with T1D. Material and Methods: A cross sectional study was carried out between January to March 2017. A total of 20 patients aged 12.25±3.74 years old with T1D and 20 healthy control group were involved. Their parents signed an informed consent. Demographic data were obtained using structured questionnaires. Physical, and laboratory examination were also performed. Blood samples were collected and serum vitamin D and IL-17 levels were measured by indirect ELISA were. Results: The serum level of vitamin D serum and IL-17 level between both groups were significantly different (p<0.001). A positive correlation between vitamin D and IL-17 levels (p<0.05; r=+0.566) was found. Conclusion: T1D is a T cell-mediated autoimmune disorder which targets and destroys insulin-producing pancreatic beta-cells. Children and adolescents with T1D show an increased level of IL-17 immunity and vitamin D deficiency. IL-17 immunity control and vitamin D supplementation could be potential targets for further development of T1D therapeutic strategies.
{"title":"Increased Level of Interleukin-17 in Children and Adolescents with Type 1 Diabetes Mellitus and its Association with Vitamin D Deficiency","authors":"H. Tjahjono, L. Farida","doi":"10.25002/tji.2019.943","DOIUrl":"https://doi.org/10.25002/tji.2019.943","url":null,"abstract":"Introduction: The up-regulation of interleukin-17 (IL-17) has been reported to be the pathogenesis of type 1 diabetes mellitus (T1D). On the other hand, vitamin D deficiency is fairly prevalent in T1D. This study aims to investigate IL-17 and vitamin D status and its correlation in children and adolescents with T1D. Material and Methods: A cross sectional study was carried out between January to March 2017. A total of 20 patients aged 12.25±3.74 years old with T1D and 20 healthy control group were involved. Their parents signed an informed consent. Demographic data were obtained using structured questionnaires. Physical, and laboratory examination were also performed. Blood samples were collected and serum vitamin D and IL-17 levels were measured by indirect ELISA were. Results: The serum level of vitamin D serum and IL-17 level between both groups were significantly different (p<0.001). A positive correlation between vitamin D and IL-17 levels (p<0.05; r=+0.566) was found. Conclusion: T1D is a T cell-mediated autoimmune disorder which targets and destroys insulin-producing pancreatic beta-cells. Children and adolescents with T1D show an increased level of IL-17 immunity and vitamin D deficiency. IL-17 immunity control and vitamin D supplementation could be potential targets for further development of T1D therapeutic strategies.","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87300369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The neuroendocrine immune network functions in a delicate balance during health and the ability to maintain this balance through disease affects the outcome of the disease. During aging, there is a general decline in each of these systems that reflects on their synergistic functions and affect homeostasis leading to age-associated diseases including cancer, autoimmunity and degenerative diseases. Immunomodulation by estrogen through cyclic menstrual variations and precipitous decline during reproductive aging, facilitates the development of several female-specific age-associated diseases such as autoimmunity, osteoporosis, cardiovascular diseases and hormone-dependent cancers. Centrally and peripherally, norepinephrine released from sympathetic innervation of lymphoid organs plays a key role in naïve T-cell regulation. Hypothalamic catecholaminergic networks play a crucial role in endocrine regulation and indirectly affect immune functions during health and disease. Immune mediators such as cytokines can cross the blood brain barrier and bind to central neurons eliciting sickness behaviour and facilitate reprogramming of energy reserves to be used to fight the disease. Monoamine oxidase inhibitors like deprenyl and synthetic drugs like donepezil have been shown to exert positive effects on the age-associated decline in the neuroendocrine-immune network by delaying peripheral degeneration and increasing immune functions. Similar beneficial effects have been observed in vitro and in vivo in rats treated with Brahmi (Bacopa monnieri) and Noni (Morinda citrifolia). Comparative analysis of the strategies for reversing age-associated immunosenescence using synthetic drugs and natural remedies have shown significant immunomodulatory effects in middle-aged and old rats through modulation of MAPK and NF-kB signaling cascades.
{"title":"Strategies to Overcome Neuroendocrine Immune Deficits in Aging: Role of Neuroendocrine-Immune Modulators and Bioactive Plant Extracts","authors":"H. P. Priyanka, R. S. Nair","doi":"10.25002/tji.2019.1027","DOIUrl":"https://doi.org/10.25002/tji.2019.1027","url":null,"abstract":"The neuroendocrine immune network functions in a delicate balance during health and the ability to maintain this balance through disease affects the outcome of the disease. During aging, there is a general decline in each of these systems that reflects on their synergistic functions and affect homeostasis leading to age-associated diseases including cancer, autoimmunity and degenerative diseases. Immunomodulation by estrogen through cyclic menstrual variations and precipitous decline during reproductive aging, facilitates the development of several female-specific age-associated diseases such as autoimmunity, osteoporosis, cardiovascular diseases and hormone-dependent cancers. Centrally and peripherally, norepinephrine released from sympathetic innervation of lymphoid organs plays a key role in naïve T-cell regulation. Hypothalamic catecholaminergic networks play a crucial role in endocrine regulation and indirectly affect immune functions during health and disease. Immune mediators such as cytokines can cross the blood brain barrier and bind to central neurons eliciting sickness behaviour and facilitate reprogramming of energy reserves to be used to fight the disease. Monoamine oxidase inhibitors like deprenyl and synthetic drugs like donepezil have been shown to exert positive effects on the age-associated decline in the neuroendocrine-immune network by delaying peripheral degeneration and increasing immune functions. Similar beneficial effects have been observed in vitro and in vivo in rats treated with Brahmi (Bacopa monnieri) and Noni (Morinda citrifolia). Comparative analysis of the strategies for reversing age-associated immunosenescence using synthetic drugs and natural remedies have shown significant immunomodulatory effects in middle-aged and old rats through modulation of MAPK and NF-kB signaling cascades.","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75802197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Rai, Akshaya Mahalakshmi Surendran, K. Nandakumar, S. Bose, Shairee Sanyal, Sumantra Mondal, Sayantanee Mukherjee, Koustav Sarkar
Introduction: Based on earlier observations on unique immunomodulatory and adjuvant functions of neem leaf glycoprotein (NLGP), investigations of this work were designed. NLGP was attempted to be used as an adjuvant for lung carcinoma-associated antigen (LCA) which not only activated macrophages but also induced macrophages to release nitric oxide (NO), a key tumoricidal agent known to regulate T-cell proliferation, cytokine production, cell signaling, and apoptosis. Materials and Methods: Macrophages, generated from peripheral blood mononuclear cells (PBMCs), were pulsed with LCA isolated from lung carcinoma cell line A549, in presence or absence of NLGP for antigen presentation. Intramacrophageal NO was estimated based on Griess reaction. Cytokine levels were estimated by ELISA. Lymphocytic proliferation was checked by MTT assay. Cytotoxic T lymphocytes (CTLs) generated cytotoxicity was tested by LDH assay. Results: NLGP potentiates immune responses during pulsation with LCA by specific lymphocytic proliferation (p<0.001) and generation of CTLs (p<0.001). LCA+NLGP treatment creates a type-1 immune environment by increasing secretion of type-1 cytokines IFN-g and IL-12 (p<0.001) and decrease in type-2 cytokines IL-4 and IL-10 (p<0.001). LCA+NLGP treatment increased the release of type-1 cytokine-dependent NO. In vitro neutralization of IFN-g/IL-12 results into drastic decrease in NO release from macrophages. Conclusion: Obtained results demonstrated the interdependence of three anti-tumor immune functions, namely, NO production, CTL generation and production of a type-1 immune response mediated through NLGP. NLGP-generated anti-LCA immune response would be an effective strategy to treat lung carcinomas.
{"title":"Neem Leaf Glycoprotein Facilitates Lung Carcinoma- Associated Antigen-Specific Anti-Cancer Immune Response Utilizing Macrophage-Mediated Antigen Presentation and Induction of Type 1 Cytokines Coupled with Nitric Oxide Production","authors":"A. Rai, Akshaya Mahalakshmi Surendran, K. Nandakumar, S. Bose, Shairee Sanyal, Sumantra Mondal, Sayantanee Mukherjee, Koustav Sarkar","doi":"10.25002/tji.2019.1012","DOIUrl":"https://doi.org/10.25002/tji.2019.1012","url":null,"abstract":"Introduction: Based on earlier observations on unique immunomodulatory and adjuvant functions of neem leaf glycoprotein (NLGP), investigations of this work were designed. NLGP was attempted to be used as an adjuvant for lung carcinoma-associated antigen (LCA) which not only activated macrophages but also induced macrophages to release nitric oxide (NO), a key tumoricidal agent known to regulate T-cell proliferation, cytokine production, cell signaling, and apoptosis. Materials and Methods: Macrophages, generated from peripheral blood mononuclear cells (PBMCs), were pulsed with LCA isolated from lung carcinoma cell line A549, in presence or absence of NLGP for antigen presentation. Intramacrophageal NO was estimated based on Griess reaction. Cytokine levels were estimated by ELISA. Lymphocytic proliferation was checked by MTT assay. Cytotoxic T lymphocytes (CTLs) generated cytotoxicity was tested by LDH assay. Results: NLGP potentiates immune responses during pulsation with LCA by specific lymphocytic proliferation (p<0.001) and generation of CTLs (p<0.001). LCA+NLGP treatment creates a type-1 immune environment by increasing secretion of type-1 cytokines IFN-g and IL-12 (p<0.001) and decrease in type-2 cytokines IL-4 and IL-10 (p<0.001). LCA+NLGP treatment increased the release of type-1 cytokine-dependent NO. In vitro neutralization of IFN-g/IL-12 results into drastic decrease in NO release from macrophages. Conclusion: Obtained results demonstrated the interdependence of three anti-tumor immune functions, namely, NO production, CTL generation and production of a type-1 immune response mediated through NLGP. NLGP-generated anti-LCA immune response would be an effective strategy to treat lung carcinomas.","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75159245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Anti-inflammatory and Anti-atherogenic Effects of Lactobacillus plantarum in Hypercholesterolemic Mice","authors":"M. Selli, A. Bermúdez-Fajardo, E. Oviedo-Orta","doi":"10.25002/TJI.2019.955","DOIUrl":"https://doi.org/10.25002/TJI.2019.955","url":null,"abstract":"","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76884756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Eken, M. Yetkin, F. Okuş, Ş. Erdem, M. Çakır, Yeşim Haliloğlu, Z. B. Azizoglu, H. Altuntaş, Meral Mirza, H. Canatan
Introduction: Th17 cells are critical mediators of pathology in several autoimmune diseases including multiple sclerosis (MS). The aim of this study was to quantify Th17 cells and-associated cytokines in the peripheral blood of relapsing remitting multiple sclerosis patients (RRMS). We also aimed to compare those levels in fingolimod-treated, and untreated patients. Material and Methods: Fifteen fingolimod administered RRMS, 9 untreated-RRMS patients and 6 healthy controls were evaluated. Their peripheral blood mononuclear cells (PBMCs) were isolated and sera separated. IL-17A+, IL-22+ and GM-CSF+ T-cells were quantified via intracellular cytokine staining after stimulation using flouresecein activated cell sorter. Serum cytokine levels from all groups were measured via enzyme-linked immunosorbent assay (ELISA). Results: Fingolimod-treated RRMS patients had reduced number of IL-17A+ (p=0.02), IL-22+ (p=0.05), and GMCSF+ (p=0.003) T cells in their peripheral blood compared to those of untreated RRMS patients. This is consistent with sequestration of lymphocytes in the secondary lymphoid organs after fingolimod use. However, the levels of same cytokines in the serum were statistically not different. Conclusions: Fingolimod treatment reduced circulating IL-17A+, IL-22+ or GM-CSF+ T cells in RRMS patients.
{"title":"Comparison of Peripheral Blood Th17 Cells and Associated Cytokines in Fingolimod-Receiving and Untreated Multiple Sclerosis Patients","authors":"A. Eken, M. Yetkin, F. Okuş, Ş. Erdem, M. Çakır, Yeşim Haliloğlu, Z. B. Azizoglu, H. Altuntaş, Meral Mirza, H. Canatan","doi":"10.25002/tji.2019.1007","DOIUrl":"https://doi.org/10.25002/tji.2019.1007","url":null,"abstract":"Introduction: Th17 cells are critical mediators of pathology in several autoimmune diseases including multiple sclerosis (MS). The aim of this study was to quantify Th17 cells and-associated cytokines in the peripheral blood of relapsing remitting multiple sclerosis patients (RRMS). We also aimed to compare those levels in fingolimod-treated, and untreated patients. Material and Methods: Fifteen fingolimod administered RRMS, 9 untreated-RRMS patients and 6 healthy controls were evaluated. Their peripheral blood mononuclear cells (PBMCs) were isolated and sera separated. IL-17A+, IL-22+ and GM-CSF+ T-cells were quantified via intracellular cytokine staining after stimulation using flouresecein activated cell sorter. Serum cytokine levels from all groups were measured via enzyme-linked immunosorbent assay (ELISA). Results: Fingolimod-treated RRMS patients had reduced number of IL-17A+ (p=0.02), IL-22+ (p=0.05), and GMCSF+ (p=0.003) T cells in their peripheral blood compared to those of untreated RRMS patients. This is consistent with sequestration of lymphocytes in the secondary lymphoid organs after fingolimod use. However, the levels of same cytokines in the serum were statistically not different. Conclusions: Fingolimod treatment reduced circulating IL-17A+, IL-22+ or GM-CSF+ T cells in RRMS patients.","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84800684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The immune system protects the inner ear from various infections. However, the fragile audiological and vestibular structures are damaged due to immune-related and inflammatory responses, thus resulting in sensorineural hearing loss. Immune-mediated sensorineural hearing loss (ISNHL) can either be of autoimmune or autoinflammatory origin, and studies have shown that ISNHL ultimately results from inflammatory responses in both the cases. Several disorders have been identified that either primarily cause hearing loss due to localized inflammation (such as Meniere’s disease) or as an additional manifestation resulting from systemic inflammation (as seen in Muckle-Well syndrome). Immune molecularand patho-mechanisms have been proposed to explain ISNHL, yet it has been an enigma. A crucial mechanism leading to immune activation and inflammation involves the increased levels of NLRP3 inflammasome-associated IL-1β and TNF-α, in resident macrophages of the inner ear. The presence of autoantibodies to inner ear antigens have been reported as a causative ISNHL and these antibodies also serve as diagnostic markers. Genetic-susceptibility to ISNHL in some individuals has been reported. ISNHL is reversible, where hearing and vestibular functions can be restored. Several studies have put forward therapeutic strategies to alleviate hearing impairment, by usage of immunosuppressive drugs, monoclonal antibodies, IL-1β and TNF-α antagonists, and NLRP3 inflammasome-inhibitors. Emerging approaches for treating autoimmune disease include altering gut microbiota, stem cell therapy and precision medicine. The present report reviews the various molecularand patho-mechanisms associated with ISNHL. It further focuses on possible therapeutic targets and the relevance in application of emerging therapeutic strategies to alleviate hearing loss.
{"title":"Immune-mediated Sensorineural Hearing Loss: Patho-Mechanisms and Therapeutic Strategies","authors":"S. ParidhyVanniya., K. Ramkumar, C. Srisailapathy","doi":"10.25002/tji.2019.1015","DOIUrl":"https://doi.org/10.25002/tji.2019.1015","url":null,"abstract":"The immune system protects the inner ear from various infections. However, the fragile audiological and vestibular structures are damaged due to immune-related and inflammatory responses, thus resulting in sensorineural hearing loss. Immune-mediated sensorineural hearing loss (ISNHL) can either be of autoimmune or autoinflammatory origin, and studies have shown that ISNHL ultimately results from inflammatory responses in both the cases. Several disorders have been identified that either primarily cause hearing loss due to localized inflammation (such as Meniere’s disease) or as an additional manifestation resulting from systemic inflammation (as seen in Muckle-Well syndrome). Immune molecularand patho-mechanisms have been proposed to explain ISNHL, yet it has been an enigma. A crucial mechanism leading to immune activation and inflammation involves the increased levels of NLRP3 inflammasome-associated IL-1β and TNF-α, in resident macrophages of the inner ear. The presence of autoantibodies to inner ear antigens have been reported as a causative ISNHL and these antibodies also serve as diagnostic markers. Genetic-susceptibility to ISNHL in some individuals has been reported. ISNHL is reversible, where hearing and vestibular functions can be restored. Several studies have put forward therapeutic strategies to alleviate hearing impairment, by usage of immunosuppressive drugs, monoclonal antibodies, IL-1β and TNF-α antagonists, and NLRP3 inflammasome-inhibitors. Emerging approaches for treating autoimmune disease include altering gut microbiota, stem cell therapy and precision medicine. The present report reviews the various molecularand patho-mechanisms associated with ISNHL. It further focuses on possible therapeutic targets and the relevance in application of emerging therapeutic strategies to alleviate hearing loss.","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87598255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introducton: Celiac disease (CD) is diagnosed with serological tests and small bowel biopsy. There is a strong link between CD and human leukocyte antigens (HLA). In this study, we aimed to determine the role of HLA alleles DQ*02 and DQ*08 in the diagnosis of pediatric CD patients and to determine the prevalence of these alleles in the population. Materials and Methods: The study included 72 school-aged celiac patients diagnosed according to serology and small bowel biopsy results, and a control group consisting of 70 unrelated individuals with no systemic disease. HLA-DQ*02 and HLA-DQ*08 typing was done using the sequence-specific primer (PCR-SSP) method. Results: The mean age of the CD patients included in the study was 10.06±2.10 years. HLA-DQ*02 frequency was significantly higher in the CD group (67%) compared to the control group (17%) (p<0.001). HLA-DQ*08 frequencies did not differ significantly between the patient and control groups (26% and 24%, respectively; p>0.05). Conclusions: Genetic risk profiles in CD are helpful for predicting susceptibility to disease and disease progression. The results of our study showed that the prevalence of HLA-DQ*02 was higher among CD patients than healthy individuals, and it was higher than the prevalence of HLA-DQ*08. Our study further supports the link between HLADQ*02 and increased risk of disease.
{"title":"Prevalence of HLA-DQ*02 and HLA-DQ*08 in Patients with Celiac Disease in Eastern Anatolia and the Diagnostic Role of HLA-DQ*02 and HLA-DQ*08 Genotyping","authors":"E. Balkan, A. Islek, E. Yaşar, H. Doğan","doi":"10.25002/TJI.2019.862","DOIUrl":"https://doi.org/10.25002/TJI.2019.862","url":null,"abstract":"Introducton: Celiac disease (CD) is diagnosed with serological tests and small bowel biopsy. There is a strong link between CD and human leukocyte antigens (HLA). In this study, we aimed to determine the role of HLA alleles DQ*02 and DQ*08 in the diagnosis of pediatric CD patients and to determine the prevalence of these alleles in the population. Materials and Methods: The study included 72 school-aged celiac patients diagnosed according to serology and small bowel biopsy results, and a control group consisting of 70 unrelated individuals with no systemic disease. HLA-DQ*02 and HLA-DQ*08 typing was done using the sequence-specific primer (PCR-SSP) method. Results: The mean age of the CD patients included in the study was 10.06±2.10 years. HLA-DQ*02 frequency was significantly higher in the CD group (67%) compared to the control group (17%) (p<0.001). HLA-DQ*08 frequencies did not differ significantly between the patient and control groups (26% and 24%, respectively; p>0.05). Conclusions: Genetic risk profiles in CD are helpful for predicting susceptibility to disease and disease progression. The results of our study showed that the prevalence of HLA-DQ*02 was higher among CD patients than healthy individuals, and it was higher than the prevalence of HLA-DQ*08. Our study further supports the link between HLADQ*02 and increased risk of disease.","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90446112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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