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Article ; Online: Phenotypic and Functional Diversities of Myeloid-Derived Suppressor Cells in Autoimmune Diseases.

Ma, Huijuan / Xia, Chang-Qing

2018 Volume 2018, Page(s) 4316584

Abstract: Myeloid-derived suppressor cells (MDSCs) are identified as a heterogeneous population of cells with the function to suppress innate as well as adaptive immune responses. The initial studies of MDSCs were primarily focused on the field of animal tumor ... ...

Abstract	Myeloid-derived suppressor cells (MDSCs) are identified as a heterogeneous population of cells with the function to suppress innate as well as adaptive immune responses. The initial studies of MDSCs were primarily focused on the field of animal tumor models or cancer patients. In cancer, MDSCs play the deleterious role to inhibit tumor immunity and to promote tumor development. Over the past few years, an increasing number of studies have investigated the role of MDSCs in autoimmune diseases. The beneficial effects of MDSCs in autoimmunity have been reported by some studies, and thus, immunosuppressive MDSCs may be a novel therapeutic target in autoimmune diseases. There are some controversial findings as well. Many questions such as the activation, differentiation, and suppressive functions of MDSCs and their roles in autoimmune diseases remain unclear. In this review, we have discussed the current understanding of MDSCs in autoimmune diseases.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; Autoimmunity/physiology ; Humans ; Myeloid-Derived Suppressor Cells/immunology
Language	English
Publishing date	2018-12-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2018/4316584
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Article ; Online: PD-1/PD-L1 Interaction Maintains Allogeneic Immune Tolerance Induced by Administration of Ultraviolet B-Irradiated Immature Dendritic Cells.

Zhang, Lanfang / Xia, Chang-Qing

Journal of immunology research

2016 Volume 2016, Page(s) 2419621

Abstract: Our previous study demonstrated that transfusion of ultraviolet B-irradiated immature dendritic cells (UVB-iDCs) induced alloantigen-specific tolerance between two different strains of mice. Programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) ...

Abstract	Our previous study demonstrated that transfusion of ultraviolet B-irradiated immature dendritic cells (UVB-iDCs) induced alloantigen-specific tolerance between two different strains of mice. Programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) have been suggested to play an important role in maintaining immune tolerance. In the present study, we seek to address whether PD-1/PD-L1 plays a role in the maintenance of UVB-iDC-induced tolerance. We first observe that the UVB-iDC-induced alloantigen-specific tolerance can be maintained for over 6 weeks. Supporting this, at 6 weeks after tolerance induction completion, alloantigen-specific tolerance is still able to be transferred to syngeneic naïve mice through adoptive transfer of CD4+ T cells. Furthermore, skin transplantation study shows that the survival of allogeneic grafts is prolonged in those tolerant recipients. Further studies show that PD-1/PD-L1 interaction is essential for maintaining the induced tolerance as blockade of PD-1/PD-L1 by anti-PD-L1 antibodies largely breaks the tolerance at both cellular and humoral immunological levels. Importantly, we show that PD-1/PD-L1 interaction in tolerant mice is also essential for controlling alloantigen-responding T cells, which have never experienced alloantigens. The above findings suggest that PD-1/PD-L1 plays a crucial role in maintaining immune tolerance induced by UVB-iDCs, as well as in actively controlling effector T cells specific to alloantigens.
MeSH term(s)	Adoptive Transfer ; Animals ; B7-H1 Antigen/metabolism ; Graft Survival/immunology ; Immune Tolerance/radiation effects ; Isoantigens/immunology ; Lymphocyte Activation/immunology ; Mice ; Programmed Cell Death 1 Receptor/metabolism ; Protein Binding ; Skin Transplantation ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Ultraviolet Rays
Chemical Substances	B7-H1 Antigen ; Isoantigens ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2016
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2817541-4
ISSN	2314-7156 ; 2314-8861
ISSN (online)	2314-7156
ISSN	2314-8861
DOI	10.1155/2016/2419621
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Article ; Online: Administration of sulfosuccinimidyl-4-[N-maleimidomethyl] cyclohexane-1-carboxylate conjugated GP100(25-33) peptide-coupled spleen cells effectively mounts antigen-specific immune response against mouse melanoma.

Chang, Xiaoli / Xia, Chang-Qing

Biochemical and biophysical research communications

2015 Volume 468, Issue 1-2, Page(s) 46–52

Abstract: It remains a top research priority to develop immunotherapeutic approaches to induce potent antigen-specific immune responses against tumors. However, in spite of some promising results, most strategies are ineffective because they generate low numbers ... ...

Abstract	It remains a top research priority to develop immunotherapeutic approaches to induce potent antigen-specific immune responses against tumors. However, in spite of some promising results, most strategies are ineffective because they generate low numbers of tumor-reactive cytotoxic T lymphocytes (CTLs). Here we designed a strategy to enhance antigen-specific immune response via administering sulfosuccinimidyl-4-[N-maleimidomethyl] cyclohexane-1-carboxylate (sulfo-SMCC)-conjugated melanoma tumor antigen GP10025-33 peptide-coupled syngeneic spleen cells in a mouse model of melanoma. We found that infusion of GP10025-33 peptide-coupled spleen cells significantly attenuated the growth of melanoma in prophylactic and therapeutic immunizations. Consistent with these findings, the adoptive transfer of spleen cells from immunized mice to naïve syngeneic mice was able to transfer anti-tumor effect, suggesting that GP10025-33 peptide-specific immune response was induced. Further studies showed that, CD8+ T cell proliferation and the frequency of interferon (IFN)-γ-producing CD8+ T cells upon ex vivo stimulation by GP10025-33 were significantly increased compared to control groups. Tumor antigen, GP10025-23 specific immune response was also confirmed by ELISpot and GP100-tetramer assays. This approach is simple, easy-handled, and efficiently delivering antigens to lymphoid tissues. Our study offers an opportunity for clinically translating this approach into tumor immunotherapy.
MeSH term(s)	Adoptive Transfer/methods ; Animals ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Immunoconjugates/administration & dosage ; Immunoconjugates/chemistry ; Immunoconjugates/therapeutic use ; Immunotherapy/methods ; Interferon-gamma/immunology ; Maleimides/administration & dosage ; Maleimides/chemistry ; Maleimides/therapeutic use ; Melanoma/immunology ; Melanoma/prevention & control ; Melanoma/therapy ; Mice ; Mice, Inbred C57BL ; Peptides/administration & dosage ; Peptides/chemistry ; Peptides/therapeutic use ; Spleen/cytology ; Spleen/immunology ; gp100 Melanoma Antigen/administration & dosage ; gp100 Melanoma Antigen/chemistry ; gp100 Melanoma Antigen/therapeutic use
Chemical Substances	Immunoconjugates ; Maleimides ; Peptides ; gp100 Melanoma Antigen ; sulfosuccinimidyl 4-(N-maleimidomethyl)cyclohexane-1-carboxylate ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2015-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2015.10.168
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Article: Administration of sulfosuccinimidyl-4-[N-maleimidomethyl] cyclohexane-1-carboxylate conjugated GP10025–33 peptide-coupled spleen cells effectively mounts antigen-specific immune response against mouse melanoma

Chang, Xiaoli / Xia, Chang-Qing

Biochemical and biophysical research communications. 2015 Dec. 04, v. 468

2015

Abstract	It remains a top research priority to develop immunotherapeutic approaches to induce potent antigen-specific immune responses against tumors. However, in spite of some promising results, most strategies are ineffective because they generate low numbers of tumor-reactive cytotoxic T lymphocytes (CTLs). Here we designed a strategy to enhance antigen-specific immune response via administering sulfosuccinimidyl-4-[N-maleimidomethyl] cyclohexane-1-carboxylate (sulfo-SMCC)-conjugated melanoma tumor antigen GP10025–33 peptide-coupled syngeneic spleen cells in a mouse model of melanoma. We found that infusion of GP10025–33 peptide-coupled spleen cells significantly attenuated the growth of melanoma in prophylactic and therapeutic immunizations. Consistent with these findings, the adoptive transfer of spleen cells from immunized mice to naïve syngeneic mice was able to transfer anti-tumor effect, suggesting that GP10025–33 peptide-specific immune response was induced. Further studies showed that, CD8+ T cell proliferation and the frequency of interferon (IFN)-γ-producing CD8+ T cells upon ex vivo stimulation by GP10025–33 were significantly increased compared to control groups. Tumor antigen, GP10025–23 specific immune response was also confirmed by ELISpot and GP100-tetramer assays. This approach is simple, easy-handled, and efficiently delivering antigens to lymphoid tissues. Our study offers an opportunity for clinically translating this approach into tumor immunotherapy.
Keywords	animal models ; antigens ; cell proliferation ; cytotoxic T-lymphocytes ; immune response ; immunotherapy ; interferons ; melanoma ; mice ; splenocytes ; tissues
Language	English
Dates of publication	2015-1204
Size	p. 46-52.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2015.10.168
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Article ; Online: Immature Dendritic Cell Therapy Confers Durable Immune Modulation in an Antigen-Dependent and Antigen-Independent Manner in Nonobese Diabetic Mice.

Lo, Jeannette / Xia, Chang-Qing / Peng, Ruihua / Clare-Salzler, Michael J

Journal of immunology research

2018 Volume 2018, Page(s) 5463879

Abstract: Dendritic cell (DC) immunotherapy has been effective for prevention of type 1 diabetes (T1D) in NOD mice but fails to protect if initiated after active autoimmunity. As autoreactivity expands inter- and intramolecularly during disease progression, we ... ...

Abstract	Dendritic cell (DC) immunotherapy has been effective for prevention of type 1 diabetes (T1D) in NOD mice but fails to protect if initiated after active autoimmunity. As autoreactivity expands inter- and intramolecularly during disease progression, we investigated whether DCs unpulsed or pulsed with
MeSH term(s)	Animals ; Antigen Presentation ; Autoantigens/immunology ; Autoantigens/metabolism ; Autoimmunity ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Dendritic Cells/physiology ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/therapy ; Disease Models, Animal ; Epitopes, T-Lymphocyte/immunology ; Epitopes, T-Lymphocyte/metabolism ; Female ; Forkhead Transcription Factors/metabolism ; Humans ; Immune Tolerance ; Immunodominant Epitopes/immunology ; Immunodominant Epitopes/metabolism ; Immunomodulation ; Immunotherapy, Adoptive/methods ; Insulin-Secreting Cells/immunology ; Insulin-Secreting Cells/metabolism ; Lymphocyte Activation ; Mice ; Mice, Inbred NOD ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Autoantigens ; Epitopes, T-Lymphocyte ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Immunodominant Epitopes
Language	English
Publishing date	2018-02-14
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2817541-4
ISSN	2314-7156 ; 2314-8861
ISSN (online)	2314-7156
ISSN	2314-8861
DOI	10.1155/2018/5463879
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Article ; Online: Effect of high glucose on cytokine production by human peripheral blood immune cells and type I interferon signaling in monocytes: Implications for the role of hyperglycemia in the diabetes inflammatory process and host defense against infection.

Hu, Ronghua / Xia, Chang-Qing / Butfiloski, Edward / Clare-Salzler, Michael

Clinical immunology (Orlando, Fla.)

2018 Volume 195, Page(s) 139–148

Abstract: The major metabolic feature of diabetes is hyperglycemia which has been linked to the diabetes inflammatory processes, and diabetes-related vulnerability to infection. In the present study, we assessed how glucose affected PBMCs in type I interferon (IFN) ...

Abstract	The major metabolic feature of diabetes is hyperglycemia which has been linked to the diabetes inflammatory processes, and diabetes-related vulnerability to infection. In the present study, we assessed how glucose affected PBMCs in type I interferon (IFN) production and subsequent signaling. We found that the moderately elevated glucose promoted, and high glucose suppressed type I IFN production, respectively. Pre-exposure to high glucose rendered monocytes more sensitive to IFN-α stimulation with heightened signaling, whereas, instantaneous addition of high glucose did not exhibit such effect. Consistent with this finding, the mRNA levels of IFN-α-induced IRF-7 in PBMCs were positively correlated with HbA1c levels of diabetes patients. Additionally, we found that high glucose promoted the production of other proinflammatory cytokines/chemokines. This study suggests that hyperglycemia may affect the inflammatory process in diabetes via promoting proinflammatory cytokines, as well as the host defense against microbial infections through impeding type I IFN production and signaling.
MeSH term(s)	Adolescent ; Adult ; Child ; Diabetes Complications/immunology ; Female ; Glucose/metabolism ; Glycated Hemoglobin A/metabolism ; Humans ; Hyperglycemia/immunology ; Immunity ; Infections/immunology ; Inflammation/immunology ; Interferon Regulatory Factor-7/genetics ; Interferon Regulatory Factor-7/metabolism ; Interferon Type I/metabolism ; Male ; Monocytes/immunology ; Sialic Acid Binding Ig-like Lectin 1/metabolism ; Signal Transduction ; THP-1 Cells ; Young Adult
Chemical Substances	Glycated Hemoglobin A ; Interferon Regulatory Factor-7 ; Interferon Type I ; SIGLEC1 protein, human ; Sialic Acid Binding Ig-like Lectin 1 ; hemoglobin A1c protein, human ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2018-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2018.06.003
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Article: Ex vivo expansion of regulatory T cells for clinical applications against graft-versus-host disease in allogeneic hematopoietic stem cell transplantation.

Zhang, Lan-fang / Xia, Chang-qing

Chinese medical journal

2013 Volume 126, Issue 23, Page(s) 4575–4582

Abstract: Objective: To review the characteristics of regulatory T cells (Tregs) and ex vivo expansion of Tregs for treatment of graft-versus-host disease (GVHD).: Data sources: The data used in this review were retrieved from PubMed (1970-2013). The terms "ex ...

Abstract	Objective: To review the characteristics of regulatory T cells (Tregs) and ex vivo expansion of Tregs for treatment of graft-versus-host disease (GVHD). Data sources: The data used in this review were retrieved from PubMed (1970-2013). The terms "ex vivo expansion", "regulatory T cell", and "graft-versus-host disease" were used for literature search. Study selection: The publications about the characteristics of Tregs, ex vivo expansion of Tregs and clinical applications of Tregs against GVHD were identified, retrieved and reviewed. Results: Tregs can be classified as natural Tregs (nTregs) and induced Tregs (iTregs). Both subsets share most Treg features. Given their immunosuppressive property, Tregs have been tested for their capability of preventing GVHD. The bottleneck of Treg therapy is the limited numbers of naturally existing Tregs. To solve this problem, ex vivo expansion of nTregs or iTregs has been executed. The initial data indicate Treg therapy is effective in reducing GVHD without compromising graft-versus-leukemia (GVL). Conclusion: Ex vivo expansion of Tregs is a reliable way to prepare sufficient number of Tregs for management of GVHD.
MeSH term(s)	Graft vs Host Disease/immunology ; Graft vs Host Disease/therapy ; Hematopoietic Stem Cell Transplantation ; Humans ; T-Lymphocytes, Regulatory/cytology
Language	English
Publishing date	2013-12
Publishing country	China
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	127089-8
ISSN	0366-6999 ; 1002-0187
ISSN	0366-6999 ; 1002-0187
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Article ; Online: Immunosuppressive CD11b+Ly6Chi monocytes in pristane-induced lupus mouse model.

Ma, Huijuan / Wan, Suigui / Xia, Chang-Qing

Journal of leukocyte biology

2016 Volume 99, Issue 6, Page(s) 1121–1129

Abstract: Myeloid-derived suppressor cells with immunosuppressive functions have been described to be associated with one of the mechanisms by which malignant tumors escape immune surveillance. However, little is known about the role of myeloid-derived suppressor ... ...

Abstract	Myeloid-derived suppressor cells with immunosuppressive functions have been described to be associated with one of the mechanisms by which malignant tumors escape immune surveillance. However, little is known about the role of myeloid-derived suppressor cells in autoimmunity. In the current study, when we attempted to characterize the peritoneal cells in pristane-induced lupus model, as reported previously, we observed that there were markedly increased CD11b(+)Ly6C(hi) monocytes. Surprisingly, this type of monocytes was almost phenotypically identical to the reported monocytic myeloid-derived suppressor cells. Further analysis on how these CD11b(+)Ly6C(hi) cells affected T cell response showed that they strongly suppressed T cell proliferation in vitro in a manner dependent on cell-cell contact, NO, and PGE2. In addition, we found that CD11b(+)Ly6C(hi) monocytes inhibited Th1 differentiation but enhanced development of forkhead box p3(+)CD4(+) regulatory T cells. Consistent with the in vitro experimental results, the in vivo adoptive cell transfer study showed that infusion of pristane-treated syngeneic CD11b(+)Ly6C(hi) monocytes significantly suppressed the production of anti-keyhole limpet hemocyanin antibodies induced by keyhole limpet hemocyanin immunization. In addition, we found that CD11b(+)Ly6C(hi) monocytes were also increased significantly in spleen and peripheral blood and showed immunosuppressive characteristics similar to their peritoneal counterparts. Our findings indicate that CD11b(+)Ly6C(hi) monocytes in a pristane-induced lupus mouse model are monocytic myeloid-derived suppressor cells instead of inflammatory monocytes, as demonstrated previously. To our knowledge, this is the first to describe myeloid-derived suppressor cells in a pristane-induced lupus mouse model, which may lead to a better understanding of the role of CD11b(+)Ly6C(hi) monocytes in this specific pristane-induced lupus model.
MeSH term(s)	Adoptive Transfer ; Animals ; Antibodies/immunology ; Antigens, Ly/metabolism ; CD11b Antigen/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Communication ; Cell Proliferation ; Dinoprostone/biosynthesis ; Disease Models, Animal ; Female ; Hemocyanins/immunology ; Immunization ; Immunosuppression ; Lupus Erythematosus, Systemic/blood ; Lupus Erythematosus, Systemic/chemically induced ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/pathology ; Mice, Inbred BALB C ; Monocytes/metabolism ; Monocytes/pathology ; Nitric Oxide/biosynthesis ; Spleen/pathology ; Terpenes
Chemical Substances	Antibodies ; Antigens, Ly ; CD11b Antigen ; Ly-6C antigen, mouse ; Terpenes ; pristane (26HZV48DT1) ; Nitric Oxide (31C4KY9ESH) ; Hemocyanins (9013-72-3) ; keyhole-limpet hemocyanin (FV4Y0JO2CX) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2016-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.3A0415-158R
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Article ; Online: Infusion of Sulfosuccinimidyl-4-[N-maleimidomethyl]cyclohexane-1-carboxylate-Conjugated MOG35-55-Coupled Spleen Cells Effectively Prevents and Reverses Experimental Autoimmune Encephalomyelitis in Mice.

Zhang, Lanfang / Guo, Yixian / Xia, Chang-Qing

Journal of immunology research

2015 Volume 2015, Page(s) 129682

Abstract: In this study, we have evaluated our recently developed method for antigen-cell coupling using sulfosuccinimidyl-4-[N-maleimidomethyl]cyclohexane-1-carboxylate (sulfo-SMCC) heterobifunctional crosslinker in prevention and reversal of experimental ... ...

Abstract	In this study, we have evaluated our recently developed method for antigen-cell coupling using sulfosuccinimidyl-4-[N-maleimidomethyl]cyclohexane-1-carboxylate (sulfo-SMCC) heterobifunctional crosslinker in prevention and reversal of experimental autoimmune encephalomyelitis (EAE). We demonstrate that infusion of MOG35-55-coupled spleen cells (MOG-SP) significantly prevents and reverses EAE. Further studies show that the protected animals exhibit significantly delayed EAE upon EAE reinduction. Moreover, adoptive transfer of CD4+ T cells from the protected mice to naïve syngeneic mice renders the recipient mice resistant to EAE induction. Unexpectedly, CD4+ T cell proliferation is similar upon ex vivo stimulation by MOG35-55 amongst all groups. However, further analysis of those proliferating CD4+ T cells shows remarkable differences in Foxp3+ regulatory T cells (70% in MOG-SP groups versus 10-25% in control groups) and in IL-17+ cells (2-3% in MOG-SP groups versus 6-9% in control groups). In addition, we discover that MOG-SP treatment also significantly attenuates MOG35-55-responding IFN-γ-producing Th1 cells. These findings suggest that MOG-SP treatment induces EAE protective MOG35-55-specific regulatory T cells and suppresses EAE pathogenic Th17 and Th1 cells. Our study provides a novel approach for antigen-based EAE immunotherapy, which can potentially be translated into clinical application for immunotherapy of multiple sclerosis.
MeSH term(s)	Adoptive Transfer ; Animals ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Encephalomyelitis, Autoimmune, Experimental/diagnosis ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/prevention & control ; Encephalomyelitis, Autoimmune, Experimental/therapy ; Epitopes, T-Lymphocyte/immunology ; Female ; Immunization ; Immunoconjugates/administration & dosage ; Lymphocyte Activation ; Maleimides ; Mice ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments ; Severity of Illness Index ; Spleen/cytology ; Spleen/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism
Chemical Substances	Epitopes, T-Lymphocyte ; Immunoconjugates ; Maleimides ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments ; myelin oligodendrocyte glycoprotein (35-55) ; sulfosuccinimidyl 4-(N-maleimidomethyl)cyclohexane-1-carboxylate
Language	English
Publishing date	2015
Publishing country	Egypt
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2817541-4
ISSN	2314-7156 ; 2314-8861
ISSN (online)	2314-7156
ISSN	2314-8861
DOI	10.1155/2015/129682
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Article ; Online: Type 1 Diabetes and Type 1 Interferonopathies: Localization of a Type 1 Common Thread of Virus Infection in the Pancreas.

Jean-Baptiste, Virginie S E / Xia, Chang-Qing / Clare-Salzler, Michael J / Horwitz, Marc S

EBioMedicine

2017 Volume 22, Page(s) 10–17

Abstract: Type 1 diabetes (T1D) has been associated with both genetic and environmental factors. Increasing incidence of T1D worldwide is prompting researchers to adopt different approaches to explain the biology of T1D, beyond the presence and activity of ... ...

Abstract	Type 1 diabetes (T1D) has been associated with both genetic and environmental factors. Increasing incidence of T1D worldwide is prompting researchers to adopt different approaches to explain the biology of T1D, beyond the presence and activity of autoreactive lymphocytes. In this review, we propose inflammatory pathways as triggers for T1D. Within the scope of those inflammatory pathways and in understanding the pathogenesis of disease, we suggest that viruses, in particular Coxsackieviruses, act by causing a type 1 interferonopathy within the pancreas and the microenvironment of the islet. As such, this connection and common thread represents an exciting platform for the development of new diagnostic, treatment and/or prevention options.
MeSH term(s)	Animals ; Cellular Microenvironment ; Coxsackievirus Infections/immunology ; Diabetes Mellitus, Type 1/immunology ; Immunity, Innate ; Interferons/metabolism ; Islets of Langerhans/immunology ; Pancreatic Diseases/immunology ; Pancreatic Diseases/virology ; Signal Transduction
Chemical Substances	Interferons (9008-11-1)
Language	English
Publishing date	2017-06-21
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2017.06.014
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