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Article ; Online: The Transcription Factor RXRα in CD11c+ APCs Regulates Intestinal Immune Homeostasis and Inflammation.

Manoharan, Indumathi / Shanmugam, Arulkumaran / Ramalingam, Malarvizhi / Patel, Nikhil / Thangaraju, Muthusamy / Ande, Satyanarayana / Pacholczyk, Rafal / Prasad, Puttur D / Manicassamy, Santhakumar

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 211, Issue 5, Page(s) 853–861

Abstract: APCs such as dendritic cells and macrophages play a pivotal role in mediating immune tolerance and restoring intestinal immune homeostasis by limiting inflammatory responses against commensal bacteria. However, cell-intrinsic molecular regulators ... ...

Abstract	APCs such as dendritic cells and macrophages play a pivotal role in mediating immune tolerance and restoring intestinal immune homeostasis by limiting inflammatory responses against commensal bacteria. However, cell-intrinsic molecular regulators critical for programming intestinal APCs to a regulatory state rather than an inflammatory state are unknown. In this study, we report that the transcription factor retinoid X receptor α (RXRα) signaling in CD11c+ APCs is essential for suppressing intestinal inflammation by imparting an anti-inflammatory phenotype. Using a mouse model of ulcerative colitis, we demonstrated that targeted deletion of RXRα in CD11c+ APCs in mice resulted in the loss of T cell homeostasis with enhanced intestinal inflammation and increased histopathological severity of colonic tissue. This was due to the increased production of proinflammatory cytokines that drive Th1/Th17 responses and decreased expression of immune-regulatory factors that promote regulatory T cell differentiation in the colon. Consistent with these findings, pharmacological activation of the RXRα pathway alleviated colitis severity in mice by suppressing the expression of inflammatory cytokines and limiting Th1/Th17 cell differentiation. These findings identify an essential role for RXRα in APCs in regulating intestinal immune homeostasis and inflammation. Thus, manipulating the RXRα pathway could provide novel opportunities for enhancing regulatory responses and dampening colonic inflammation.
MeSH term(s)	Animals ; Mice ; Colitis ; Colon ; Cytokines/metabolism ; Homeostasis ; Inflammation ; Intestinal Mucosa ; Intestines/pathology ; Mice, Inbred C57BL ; Retinoid X Receptor alpha ; Transcription Factors/metabolism
Chemical Substances	Cytokines ; Retinoid X Receptor alpha ; Transcription Factors
Language	English
Publishing date	2023-07-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2200909
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Article ; Online: The Simple prEservatioN of Single cElls method for cryopreservation enables the generation of single-cell immune profiles from whole blood.

Satpathy, Sarthak / Thomas, Beena E / Pilcher, William J / Bakhtiari, Mojtaba / Ponder, Lori A / Pacholczyk, Rafal / Prahalad, Sampath / Bhasin, Swati S / Munn, David H / Bhasin, Manoj K

Frontiers in immunology

2023 Volume 14, Page(s) 1271800

Abstract: Introduction: Current multistep methods utilized for preparing and cryopreserving single-cell suspensions from blood samples for single-cell RNA sequencing (scRNA-seq) are time-consuming, requiring trained personnel and special equipment, so limiting ... ...

Abstract	Introduction: Current multistep methods utilized for preparing and cryopreserving single-cell suspensions from blood samples for single-cell RNA sequencing (scRNA-seq) are time-consuming, requiring trained personnel and special equipment, so limiting their clinical adoption. We developed a method, Simple prEservatioN of Single cElls (SENSE), for single-step cryopreservation of whole blood (WB) along with granulocyte depletion during single-cell assay, to generate high quality single-cell profiles (SCP). Methods: WB was cryopreserved using the SENSE method and peripheral blood mononuclear cells (PBMCs) were isolated and cryopreserved using the traditional density-gradient method (PBMC method) from the same blood sample (n=6). The SCPs obtained from both methods were processed using a similar pipeline and quality control parameters. Further, entropy calculation, differential gene expression, and cellular communication analysis were performed to compare cell types and subtypes from both methods. Results: Highly viable (86.3 ± 1.51%) single-cell suspensions (22,353 cells) were obtained from the six WB samples cryopreserved using the SENSE method. In-depth characterization of the scRNA-seq datasets from the samples processed with the SENSE method yielded high-quality profiles of lymphoid and myeloid cell types which were in concordance with the profiles obtained with classical multistep PBMC method processed samples. Additionally, the SENSE method cryopreserved samples exhibited significantly higher T-cell enrichment, enabling deeper characterization of T-cell subtypes. Overall, the SENSE and PBMC methods processed samples exhibited transcriptional, and cellular communication network level similarities across cell types with no batch effect except in myeloid lineage cells. Discussion: Comparative analysis of scRNA-seq datasets obtained with the two cryopreservation methods i.e., SENSE and PBMC methods, yielded similar cellular and molecular profiles, confirming the suitability of the former method's incorporation in clinics/labs for cryopreserving and obtaining high-quality single-cells for conducting critical translational research.
MeSH term(s)	Leukocytes, Mononuclear ; Cryopreservation/methods ; Quality Control
Language	English
Publishing date	2023-11-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1271800
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Article ; Online: A Tryptophan-Deficient Diet Induces Gut Microbiota Dysbiosis and Increases Systemic Inflammation in Aged Mice.

Yusufu, Ibrahim / Ding, Kehong / Smith, Kathryn / Wankhade, Umesh D / Sahay, Bikash / Patterson, G Taylor / Pacholczyk, Rafal / Adusumilli, Satish / Hamrick, Mark W / Hill, William D / Isales, Carlos M / Fulzele, Sadanand

International journal of molecular sciences

2021 Volume 22, Issue 9

Abstract: The gut microflora is a vital component of the gastrointestinal (GI) system that regulates local and systemic immunity, inflammatory response, the digestive system, and overall health. Older people commonly suffer from inadequate nutrition or poor diets, ...

Abstract	The gut microflora is a vital component of the gastrointestinal (GI) system that regulates local and systemic immunity, inflammatory response, the digestive system, and overall health. Older people commonly suffer from inadequate nutrition or poor diets, which could potentially alter the gut microbiota. The essential amino acid (AA) tryptophan (TRP) is a vital diet component that plays a critical role in physiological stress responses, neuropsychiatric health, oxidative systems, inflammatory responses, and GI health. The present study investigates the relationship between varied TRP diets, the gut microbiome, and inflammatory responses in an aged mouse model. We fed aged mice either a TRP-deficient (0.1%), TRP-recommended (0.2%), or high-TRP (1.25%) diet for eight weeks and observed changes in the gut bacterial environment and the inflammatory responses via cytokine analysis (IL-1a, IL-6, IL-17A, and IL-27). The mice on the TRP-deficient diets showed changes in their bacterial abundance of Coriobacteriia class,
MeSH term(s)	Aging/blood ; Aging/pathology ; Animals ; Bacteria/classification ; Biodiversity ; Cytokines/blood ; Diet ; Feces/microbiology ; Gastrointestinal Microbiome ; Inflammation/blood ; Inflammation/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Phylogeny ; Tryptophan/deficiency
Chemical Substances	Cytokines ; Tryptophan (8DUH1N11BX)
Language	English
Publishing date	2021-05-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22095005
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Article ; Online: Stimulator of interferon genes agonists attenuate type I diabetes progression in NOD mice.

Lemos, Henrique / Mohamed, Eslam / Huang, Lei / Chandler, Phillip R / Ou, Rong / Pacholczyk, Rafal / Mellor, Andrew L

Immunology

2019 Volume 158, Issue 4, Page(s) 353–361

Abstract: Reagents that activate the signaling adaptor stimulator of interferon genes (STING) suppress experimentally induced autoimmunity in murine models of multiple sclerosis and arthritis. In this study, we evaluated STING agonists as potential reagents to ... ...

Abstract	Reagents that activate the signaling adaptor stimulator of interferon genes (STING) suppress experimentally induced autoimmunity in murine models of multiple sclerosis and arthritis. In this study, we evaluated STING agonists as potential reagents to inhibit spontaneous autoimmune type I diabetes (T1D) onset in non-obese diabetic (NOD) female mice. Treatments with DNA nanoparticles (DNPs), which activate STING when cargo DNA is sensed, delayed T1D onset and reduced T1D incidence when administered before T1D onset. DNP treatment elevated indoleamine 2,3 dioxygenase (IDO) activity, which regulates T-cell immunity, in spleen, pancreatic lymph nodes and pancreas of NOD mice. Therapeutic responses to DNPs were partially reversed by inhibiting IDO and DNP treatment synergized with insulin therapy to further delay T1D onset and reduce T1D incidence. Treating pre-diabetic NOD mice with cyclic guanyl-adenyl dinucleotide (cGAMP) to activate STING directly delayed T1D onset and stimulated interferon-αβ (IFN-αβ), while treatment with cyclic diguanyl nucleotide (cdiGMP) did not delay T1D onset or induce IFN-αβ in NOD mice. DNA sequence analyses revealed that NOD mice possess a STING polymorphism that may explain differential responses to cGAMP and cdiGMP. In summary, STING agonists attenuate T1D progression and DNPs enhance therapeutic responses to insulin therapy.
MeSH term(s)	Animals ; Cyclic GMP/analogs & derivatives ; Cyclic GMP/metabolism ; DNA/chemistry ; DNA/therapeutic use ; Diabetes Mellitus, Type 1/drug therapy ; Disease Models, Animal ; Drug Synergism ; Female ; Humans ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Insulin/therapeutic use ; Membrane Proteins/agonists ; Membrane Proteins/genetics ; Mice ; Mice, Inbred NOD ; Nanoparticles/chemistry ; Nanoparticles/therapeutic use ; Nucleotides, Cyclic/metabolism ; Polymorphism, Genetic ; T-Lymphocytes/immunology ; Up-Regulation
Chemical Substances	Indoleamine-Pyrrole 2,3,-Dioxygenase ; Insulin ; Membrane Proteins ; Nucleotides, Cyclic ; Sting1 protein, mouse ; cyclic guanosine monophosphate-adenosine monophosphate ; bis(3',5')-cyclic diguanylic acid (61093-23-0) ; DNA (9007-49-2) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2019-10-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.13122
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Article ; Online: Long-term sustainable dendritic cell-specific depletion murine model for periodontitis research.

Finger Stadler, Amanda / Patel, Mitulkumar / Pacholczyk, Rafal / Cutler, Christopher W / Arce, Roger M

Journal of immunological methods

2017 Volume 449, Page(s) 7–14

Abstract: Dendritic cells (DCs) are specialized antigen-presenting cells that play a pivotal role in the pathogenesis of periodontitis. The use of animal models to study the role of DCs in periodontitis has been limited by lack of a method for sustained depletion ... ...

Abstract	Dendritic cells (DCs) are specialized antigen-presenting cells that play a pivotal role in the pathogenesis of periodontitis. The use of animal models to study the role of DCs in periodontitis has been limited by lack of a method for sustained depletion of DCs. Hence, the objectives of this study were to validate the zDC-DTR knockin mouse model of conventional DCs (cDCs) depletion, as well as to investigate whether this depletion could be sustained long enough to induce alveolar bone loss in this model. zDC-DTR mice were treated with different dose regimens of diphtheria toxin (DT) to determine survival rate. A loading DT dose of 20ng/bw, followed and maintained with doses of 10ng/bm every 3days for up to 4weeks demonstrated 80% survival. Animals were weighed weekly and peripheral blood was obtained to confirm normal neutrophil counts. Five animals per group were euthanized at baseline, 24h, 1 and 4weeks. Bone marrow (BM), spleen (SP) and gingival tissue (GT) were harvested, and cells were isolated, separated and stained for Pre-DCs precursors (CD45R
MeSH term(s)	Animals ; Bone Marrow Cells/immunology ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Diphtheria Toxin/administration & dosage ; Diphtheria Toxin/immunology ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Periodontitis/immunology ; Spleen/cytology ; Spleen/immunology ; Time Factors
Chemical Substances	Diphtheria Toxin
Language	English
Publishing date	2017-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	120142-6
ISSN	1872-7905 ; 0022-1759
ISSN (online)	1872-7905
ISSN	0022-1759
DOI	10.1016/j.jim.2017.06.007
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Article ; Online: IRAK1-regulated IFN-γ signaling induces MDSC to facilitate immune evasion in FGFR1-driven hematological malignancies.

Cai, Baohuan / Liu, Yun / Chong, Yating / Zhang, Hualei / Matsunaga, Atsuko / Fang, Xuexiu / Pacholczyk, Rafal / Zhou, Gang / Cowell, John K / Hu, Tianxiang

Molecular cancer

2021 Volume 20, Issue 1, Page(s) 165

Abstract: Background: Stem Cell leukemia/lymphoma syndrome (SCLL) presents as a myeloproliferative disease which can progress to acute myeloid leukemia and is associated with the coincident development of B-cell and T-cell lymphomas. SCLL is driven by the ... ...

Abstract	Background: Stem Cell leukemia/lymphoma syndrome (SCLL) presents as a myeloproliferative disease which can progress to acute myeloid leukemia and is associated with the coincident development of B-cell and T-cell lymphomas. SCLL is driven by the constitutive activation of fibroblast growth factor receptor-1 (FGFR1) as a result of chromosome translocations with poor outcome. Mouse models have been developed which faithfully recapitulate the human disease and have been used to characterize the molecular genetic events that are associated with development and progression of the disease. Methods: CRISPR/Cas9 approaches were used to generate SCLL cells null for Interleukin receptor associated kinase 1 (IRAK1) and interferon gamma (IFNG) which were introduced into syngeneic hosts through tail vein injection. Development of the disease and changes in immune cell composition and activity were monitored using flow cytometry. Bead-based immunoassays were used to compare the cytokine and chemokine profiles of control and knock out (KO) cells. Antibody mediated, targeted depletion of T cell and MDSCs were performed to evaluate their role in antitumor immune responses. Results: In SCLL, FGFR1 activation silences miR-146b-5p through DNMT1-mediated promoter methylation, which derepresses the downstream target IRAK1. IRAK1 KO SCLL cells were xenografted into immunocompetent syngeneic mice where the typical rapid progression of disease was lost and the mice remained disease free. IRAK1 in this system has no effect on cell cycle progression or apoptosis and robust growth of the KO cells in immunodeficient mice suggested an effect on immune surveillance. Depletion of T-cells in immunocompetent mice restored leukemogenesis of the KO cells, and tumor killing assays confirmed the role of T cells in tumor clearance. Analysis of the immune cell profile in mice transplanted with the IRAK1 expressing mock control (MC) cells shows that there is an increase in levels of myeloid-derived suppressor cells (MDSCs) with a concomitant decrease in CD4+/CD8+ T-cell levels. MDSC suppression assays and depletion experiments showed that these MDSCs were responsible for suppression of the T cell mediated leukemia cell elimination. Immuno-profiling of a panel of secreted cytokines and chemokines showed that activation of IFN-γ is specifically impaired in the KO cells. In vitro and in vivo expression assays and engraftment with interferon gamma receptor-1 (IFNGR1) null mice and IFNG KO SCLL cells, showed the leukemia cells produced IFN-γ directly participating in the induction of MDSCs to establish immune evasion. Inhibition of IRAK1 using pacritinib suppresses leukemogenesis with impaired induction of MDSCs and attenuated suppression of CD4+/CD8+ T-cells. Conclusions: IRAK1 orchestrates a previously unknown FGFR1-directed immune escape mechanism in SCLL, through induction of MDSCs via regulation of IFN-γ signaling from leukemia cells, and targeting IRAK1 may provide a means of suppressing tumor growth in this syndrome by restoring immune surveillance.
MeSH term(s)	Biomarkers ; Disease Susceptibility ; Gene Expression Regulation, Neoplastic ; Hematologic Neoplasms/etiology ; Hematologic Neoplasms/metabolism ; Hematologic Neoplasms/pathology ; Humans ; Immune Evasion ; Interferon-gamma/metabolism ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Myeloid-Derived Suppressor Cells/immunology ; Myeloid-Derived Suppressor Cells/metabolism ; Receptor, Fibroblast Growth Factor, Type 1/genetics ; Receptor, Fibroblast Growth Factor, Type 1/metabolism ; Signal Transduction
Chemical Substances	Biomarkers ; Interferon-gamma (82115-62-6) ; FGFR1 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1) ; IRAK1 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-12-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2091373-4
ISSN	1476-4598 ; 1476-4598
ISSN (online)	1476-4598
ISSN	1476-4598
DOI	10.1186/s12943-021-01460-1
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Article ; Online: The T-cell receptor repertoire of regulatory T cells.

Pacholczyk, Rafal / Kern, Joanna

Immunology

2009 Volume 125, Issue 4, Page(s) 450–458

Abstract: The CD4(+) CD25(+) regulatory population of T cells (Treg cells), which expresses the forkhead family transcription factor (Foxp3), is the key component of the peripheral tolerance mechanism that protects us from a variety of autoimmune diseases. ... ...

Abstract	The CD4(+) CD25(+) regulatory population of T cells (Treg cells), which expresses the forkhead family transcription factor (Foxp3), is the key component of the peripheral tolerance mechanism that protects us from a variety of autoimmune diseases. Experimental evidence shows that Treg cells recognize a wide range of antigenic specificities with increased reactivity to self antigens, although the affinity of these interactions remains to be further defined. The Treg repertoire is highly diverse with a distinct set of T-cell receptors (TCRs), and yet is overlapping to some extent with the repertoire of conventional T cells (Tconv cells). The majority of Treg cells are generated in the thymus. However, the role of the TCR specificity in directing thymic precursors to become Treg or Tconv cells remains unclear. On the one hand, the higher self reactivity of Treg cells and utilization of different TCRs in Treg and Tconv repertoires suggest that in TCR interactions an initial decision is made about the 'suitability' of a developing thymocyte to become a Treg cell. On the other hand, as Treg cells can recognize a wide range of foreign antigens, have a diverse TCR repertoire, and show some degree of overlap with Tconv cells, the signals through the TCR may be complementary to the TCR-independent process that generates precursors of Treg cells. In this review, we discuss how different features of the Treg repertoire influence our understanding of Treg specificities and the role of self reactivity in the generation of this population.
MeSH term(s)	Animals ; Epitopes ; Forkhead Transcription Factors/immunology ; Humans ; Major Histocompatibility Complex ; Receptors, Antigen, T-Cell/immunology ; Self Tolerance/immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology
Chemical Substances	Epitopes ; FOXP3 protein, human ; Forkhead Transcription Factors ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2009-01-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/j.1365-2567.2008.02992.x
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Article ; Online: A Tryptophan-Deficient Diet Induces Gut Microbiota Dysbiosis and Increases Systemic Inflammation in Aged Mice

Ibrahim Yusufu / Kehong Ding / Kathryn Smith / Umesh D. Wankhade / Bikash Sahay / G. Taylor Patterson / Rafal Pacholczyk / Satish Adusumilli / Mark W. Hamrick / William D. Hill / Carlos M. Isales / Sadanand Fulzele

International Journal of Molecular Sciences, Vol 22, Iss 5005, p

2021 Volume 5005

Abstract	The gut microflora is a vital component of the gastrointestinal (GI) system that regulates local and systemic immunity, inflammatory response, the digestive system, and overall health. Older people commonly suffer from inadequate nutrition or poor diets, which could potentially alter the gut microbiota. The essential amino acid (AA) tryptophan (TRP) is a vital diet component that plays a critical role in physiological stress responses, neuropsychiatric health, oxidative systems, inflammatory responses, and GI health. The present study investigates the relationship between varied TRP diets, the gut microbiome, and inflammatory responses in an aged mouse model. We fed aged mice either a TRP-deficient (0.1%), TRP-recommended (0.2%), or high-TRP (1.25%) diet for eight weeks and observed changes in the gut bacterial environment and the inflammatory responses via cytokine analysis (IL-1a, IL-6, IL-17A, and IL-27). The mice on the TRP-deficient diets showed changes in their bacterial abundance of Coriobacteriia class, Acetatifactor genus, Lachnospiraceae family, Enterococcus faecalis species, Clostridium sp genus, and Oscillibacter genus. Further, these mice showed significant increases in IL-6, IL-17A, and IL-1a and decreased IL-27 levels. These data suggest a direct association between dietary TRP content, the gut microbiota microenvironment, and inflammatory responses in aged mice models.
Keywords	tryptophan ; systemic inflammation ; dysbiosis ; gut ; microbiota ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	590
Language	English
Publishing date	2021-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article: Dendritic cell derived exosomes loaded with immunoregulatory cargo reprogram local immune responses and inhibit degenerative bone disease

Elashiry, Mahmoud / Elashiry, Mohamed M / Elsayed, Ranya / Rajendran, Mythily / Auersvald, Carol / Zeitoun, Rana / Rashid, Mohammad H / Ara, Roxan / Meghil, Mohamed M / Liu, Yutao / Arbab, Ali S / Arce, Roger M / Hamrick, Mark / Elsalanty, Mohammed / Brendan, Marshall / Pacholczyk, Rafal / Cutler, Christopher W

Journal of extracellular vesicles

2020 Volume 9, Issue 1, Page(s) 1795362

Abstract: Chronic bone degenerative diseases represent a major threat to the health and well-being of the population, particularly those with advanced age. This study isolated exosomes (EXO), natural nano-particles, from dendritic cells, the "directors" of the ... ...

Abstract	Chronic bone degenerative diseases represent a major threat to the health and well-being of the population, particularly those with advanced age. This study isolated exosomes (EXO), natural nano-particles, from dendritic cells, the "directors" of the immune response, to examine the immunobiology of DC EXO in mice, and their ability to reprogram immune cells responsible for experimental alveolar bone loss
Language	English
Publishing date	2020-08-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2683797-3
ISSN	2001-3078
ISSN	2001-3078
DOI	10.1080/20013078.2020.1795362
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Article ; Online: Reduction of T cell receptor diversity in NOD mice prevents development of type 1 diabetes but not Sjögren's syndrome.

Kern, Joanna / Drutel, Robert / Leanhart, Silvia / Bogacz, Marek / Pacholczyk, Rafal

PloS one

2014 Volume 9, Issue 11, Page(s) e112467

Abstract: Non-obese diabetic (NOD) mice are well-established models of independently developing spontaneous autoimmune diseases, Sjögren's syndrome (SS) and type 1 diabetes (T1D). The key determining factor for T1D is the strong association with particular MHCII ... ...

Abstract	Non-obese diabetic (NOD) mice are well-established models of independently developing spontaneous autoimmune diseases, Sjögren's syndrome (SS) and type 1 diabetes (T1D). The key determining factor for T1D is the strong association with particular MHCII molecule and recognition by diabetogenic T cell receptor (TCR) of an insulin peptide presented in the context of I-Ag7 molecule. For SS the association with MHCII polymorphism is weaker and TCR diversity involved in the onset of the autoimmune phase of SS remains poorly understood. To compare the impact of TCR diversity reduction on the development of both diseases we generated two lines of TCR transgenic NOD mice. One line expresses transgenic TCRβ chain originated from a pathogenically irrelevant TCR, and the second line additionally expresses transgenic TCRαmini locus. Analysis of TCR sequences on NOD background reveals lower TCR diversity on Treg cells not only in the thymus, but also in the periphery. This reduction in diversity does not affect conventional CD4+ T cells, as compared to the TCRmini repertoire on B6 background. Interestingly, neither transgenic TCRβ nor TCRmini mice develop diabetes, which we show is due to lack of insulin B:9-23 specific T cells in the periphery. Conversely SS develops in both lines, with full glandular infiltration, production of autoantibodies and hyposalivation. It shows that SS development is not as sensitive to limited availability of TCR specificities as T1D, which suggests wider range of possible TCR/peptide/MHC interactions driving autoimmunity in SS.
MeSH term(s)	Amino Acid Sequence ; Animals ; Autoantibodies/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/immunology ; Flow Cytometry ; Genetic Variation/immunology ; Insulin/genetics ; Insulin/immunology ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Mice, Transgenic ; Molecular Sequence Data ; Peptide Fragments/genetics ; Peptide Fragments/immunology ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Salivary Glands/immunology ; Salivary Glands/metabolism ; Sjogren's Syndrome/genetics ; Sjogren's Syndrome/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Xerostomia/immunology
Chemical Substances	Autoantibodies ; Insulin ; Peptide Fragments ; Receptors, Antigen, T-Cell ; Receptors, Antigen, T-Cell, alpha-beta ; insulin B (9-23)
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0112467
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Inter-library loan at ZB MED

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Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED