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  1. Article ; Online: Inflammasomes in the pathophysiology of autoinflammatory syndromes.

    Tartey, Sarang / Kanneganti, Thirumala-Devi

    Journal of leukocyte biology

    2019  Volume 107, Issue 3, Page(s) 379–391

    Abstract: Inflammasomes are a specialized group of intracellular sensors that are key components of the host innate immune system. Autoinflammatory diseases are disorders of the innate immune system that are characterized by recurrent inflammation and serious ... ...

    Abstract Inflammasomes are a specialized group of intracellular sensors that are key components of the host innate immune system. Autoinflammatory diseases are disorders of the innate immune system that are characterized by recurrent inflammation and serious complications. Dysregulation of the inflammasome is associated with the onset and progression of several autoinflammatory and autoimmune diseases, including cryopyrin-associated periodic fever syndrome, familial Mediterranean fever, rheumatoid arthritis, and systemic lupus erythematosus. In this review, we discuss the involvement of various inflammasome components in the regulation of autoinflammatory disorders and describe the manifestations of these autoinflammatory diseases caused by inflammasome activation.
    MeSH term(s) Autoimmune Diseases/physiopathology ; Humans ; Inflammasomes/metabolism ; Inflammation/physiopathology ; Interleukin-1/metabolism ; Models, Biological ; Syndrome
    Chemical Substances Inflammasomes ; Interleukin-1
    Language English
    Publishing date 2019-10-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1002/JLB.3MIR0919-191R
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  2. Article ; Online: Differential role of the NLRP3 inflammasome in infection and tumorigenesis.

    Tartey, Sarang / Kanneganti, Thirumala-Devi

    Immunology

    2019  Volume 156, Issue 4, Page(s) 329–338

    Abstract: Dysregulated inflammation is one of the hallmarks of cancer initiation and progression. Emerging evidence indicates that inflammasomes play a central role in regulating immune cell functions in various infections and cancer. Inflammasomes are multimeric ... ...

    Abstract Dysregulated inflammation is one of the hallmarks of cancer initiation and progression. Emerging evidence indicates that inflammasomes play a central role in regulating immune cell functions in various infections and cancer. Inflammasomes are multimeric complexes consisting of nucleotide-binding oligomerization domain (NOD) -like receptors (NLRs). Among the NLRs, NOD1, NOD2 and NLRP3 respond to a variety of endogenous (i.e. damage-associated molecular patterns) and exogenous (i.e. pathogen-associated molecular patterns) stimuli. The NLRP3 inflammasome is associated with the onset and progression of autoinflammatory and autoimmune diseases, including metabolic disorders, multiple sclerosis, inflammatory bowel disease, and cryopyrin-associated periodic fever syndrome. NLRP3 is also associated with a wide variety of infections and tumorigenesis that are closely correlated with chemotherapy response and prognosis. In this review, we explore the rapidly expanding body of research on the expression and functions of NLRP3 in infections and cancers and outline novel inhibitors targeting the NLRP3 inflammasome that could be developed as therapeutic alternatives to current anticancer treatment.
    MeSH term(s) Animals ; Carcinogenesis/drug effects ; Carcinogenesis/immunology ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Humans ; Infections/drug therapy ; Infections/immunology ; Infections/metabolism ; Inflammasomes/drug effects ; Inflammasomes/immunology ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
    Language English
    Publishing date 2019-02-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/imm.13046
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  3. Article ; Online: Pathogen recognition and Toll-like receptor targeted therapeutics in innate immune cells.

    Tartey, Sarang / Takeuchi, Osamu

    International reviews of immunology

    2017  Volume 36, Issue 2, Page(s) 57–73

    Abstract: The innate immune system deploys a variety of pattern-recognition receptors (PRRs) which include Toll-like receptors (TLRs), RIG-I-like receptors, NOD-like receptors, and C-type lectin receptors to detect the invasion of pathogens and initiate protective ...

    Abstract The innate immune system deploys a variety of pattern-recognition receptors (PRRs) which include Toll-like receptors (TLRs), RIG-I-like receptors, NOD-like receptors, and C-type lectin receptors to detect the invasion of pathogens and initiate protective responses. The intercellular and intracellular orchestration of signals from different PRRs, their endogenous or microbial ligands and accessory molecules determine the stimulatory or inhibitory responses. Progressing over the last two decades, considerable research on the molecular mechanisms underlying host-pathogen interactions has led to a paradigm shift of our understanding of TLR signaling in the innate immune system. Given that a significant amount of evidence implicates TLRs in the pathogenesis of immune diseases and cancer, and their activation occurs early in the inflammatory cascade, they are attractive targets for novel therapeutic agents. In this review, we discuss the recent advances in TLR signaling cross talks and the mechanism of pathogen recognition with special emphasis on the role of TLRs in tumor immunity and TLR-targeted therapeutics.
    Language English
    Publishing date 2017-03-04
    Publishing country England
    Document type Journal Article
    ZDB-ID 632825-8
    ISSN 1563-5244 ; 1545-5858 ; 0883-0185
    ISSN (online) 1563-5244 ; 1545-5858
    ISSN 0883-0185
    DOI 10.1080/08830185.2016.1261318
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  4. Article ; Online: A MyD88/IL1R Axis Regulates PD-1 Expression on Tumor-Associated Macrophages and Sustains Their Immunosuppressive Function in Melanoma.

    Tartey, Sarang / Neale, Geoffrey / Vogel, Peter / Malireddi, R K Subbarao / Kanneganti, Thirumala-Devi

    Cancer research

    2021  Volume 81, Issue 9, Page(s) 2358–2372

    Abstract: Macrophages are critical mediators of tissue homeostasis, cell proliferation, and tumor metastasis. Tumor-associated macrophages (TAM) are generally associated with tumor-promoting immunosuppressive functions in solid tumors. Here, we examined the ... ...

    Abstract Macrophages are critical mediators of tissue homeostasis, cell proliferation, and tumor metastasis. Tumor-associated macrophages (TAM) are generally associated with tumor-promoting immunosuppressive functions in solid tumors. Here, we examined the transcriptional landscape of adaptor molecules downstream of Toll-like receptors in human cancers and found that higher expression of
    MeSH term(s) Animals ; Cell Line, Tumor ; Disease Models, Animal ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immune Tolerance/genetics ; Male ; Melanoma/immunology ; Melanoma/pathology ; Mice ; Mice, Knockout ; Myeloid Differentiation Factor 88/deficiency ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Programmed Cell Death 1 Receptor/metabolism ; Receptors, Interleukin-1/genetics ; Receptors, Interleukin-1/metabolism ; Signal Transduction/genetics ; Skin Neoplasms/immunology ; Skin Neoplasms/pathology ; Tumor-Associated Macrophages/immunology
    Chemical Substances MYD88 protein, human ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Receptors, Interleukin-1
    Language English
    Publishing date 2021-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-20-3510
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  5. Article: Akirin2-Mediated Transcriptional Control by Recruiting SWI/SNF Complex in B Cells.

    Tartey, Sarang / Takeuchi, Osamu

    Critical reviews in immunology

    2016  Volume 36, Issue 5, Page(s) 395–406

    Abstract: Extensive studies in last decade have demonstrated that dynamic control of gene transcription is key in the regulation of inflammatory responses. Although signaling pathways and transcription factors have a central role, growing evidence for the ... ...

    Abstract Extensive studies in last decade have demonstrated that dynamic control of gene transcription is key in the regulation of inflammatory responses. Although signaling pathways and transcription factors have a central role, growing evidence for the involvement of chromatin in the regulation of gene expression in immune cells has uncovered an evolutionarily conserved role of pathogen recognition and epigenetic regulation. The substantial potential of these responses to drive pathological inflammation and tissue damage highlights the need for rigorous control of these responses. Recently, an evolutionarily conserved nuclear factor, Akirin2, has been identified as an essential link between nuclear factor-κB and chromatin remodelers for transcriptional regulation in macrophages and B cells. In this review, we discuss current understanding of the molecular mechanisms that have instrumental roles in governing the inflammatory response with special emphasis on Akirin2 in B cells.
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1353116-5
    ISSN 1040-8401
    ISSN 1040-8401
    DOI 10.1615/CritRevImmunol.2017019629
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  6. Article ; Online: Chromatin Remodeling and Transcriptional Control in Innate Immunity: Emergence of Akirin2 as a Novel Player.

    Tartey, Sarang / Takeuchi, Osamu

    Biomolecules

    2015  Volume 5, Issue 3, Page(s) 1618–1633

    Abstract: Transcriptional regulation of inflammatory gene expression has been at the forefront of studies of innate immunity and is coordinately regulated by transcription factors, including NF-κB, and chromatin modifiers. The growing evidence for involvement of ... ...

    Abstract Transcriptional regulation of inflammatory gene expression has been at the forefront of studies of innate immunity and is coordinately regulated by transcription factors, including NF-κB, and chromatin modifiers. The growing evidence for involvement of chromatin in the regulation of gene expression in innate immune cells, has uncovered an evolutionarily conserved role of microbial sensing and chromatin remodeling. Toll-like receptors and RIG-I-like receptors trigger these signaling pathways leading to transcriptional expression of a set of genes involved in inflammation. Tightly regulated control of this gene expression is a paramount, and often foremost, goal of most biological endeavors. In this review, we will discuss the recent progress about the molecular mechanisms governing control of pro-inflammatory gene expression by an evolutionarily conserved novel nuclear protein Akirin2 in macrophages and its emergence as an essential link between NF-κB and chromatin remodelers for transcriptional regulation.
    MeSH term(s) Animals ; Chromatin Assembly and Disassembly ; Gene Expression Regulation ; Humans ; Immunity, Innate/genetics ; NF-kappa B/metabolism ; Nuclear Proteins/metabolism ; Transcription, Genetic
    Chemical Substances NF-kappa B ; Nuclear Proteins
    Language English
    Publishing date 2015-07-22
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom5031618
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  7. Article ; Online: Ets-2 deletion in myeloid cells attenuates IL-1α-mediated inflammatory disease caused by a Ptpn6 point mutation.

    Tartey, Sarang / Gurung, Prajwal / Karki, Rajendra / Burton, Amanda / Hertzog, Paul / Kanneganti, Thirumala-Devi

    Cellular & molecular immunology

    2020  Volume 18, Issue 7, Page(s) 1798–1808

    Abstract: The SHP-1 protein encoded by the Ptpn6 gene has been extensively studied in hematopoietic cells in the context of inflammation. A point mutation in this gene ( ... ...

    Abstract The SHP-1 protein encoded by the Ptpn6 gene has been extensively studied in hematopoietic cells in the context of inflammation. A point mutation in this gene (Ptpn6
    MeSH term(s) Animals ; Inflammation/pathology ; Interleukin-1alpha/metabolism ; Mice ; Neutrophils/metabolism ; Point Mutation ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/metabolism ; Proto-Oncogene Protein c-ets-2/genetics
    Chemical Substances Ets2 protein, mouse ; Il1a protein, mouse ; Interleukin-1alpha ; Proto-Oncogene Protein c-ets-2 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48) ; Ptpn6 protein, mouse (EC 3.1.3.48)
    Language English
    Publishing date 2020-03-19
    Publishing country China
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2435097-7
    ISSN 2042-0226 ; 1672-7681
    ISSN (online) 2042-0226
    ISSN 1672-7681
    DOI 10.1038/s41423-020-0398-7
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  8. Article ; Online: Chromatin Remodeling and Transcriptional Control in Innate Immunity

    Sarang Tartey / Osamu Takeuchi

    Biomolecules, Vol 5, Iss 3, Pp 1618-

    Emergence of Akirin2 as a Novel Player

    2015  Volume 1633

    Abstract: Transcriptional regulation of inflammatory gene expression has been at the forefront of studies of innate immunity and is coordinately regulated by transcription factors, including NF-κB, and chromatin modifiers. The growing evidence for involvement of ... ...

    Abstract Transcriptional regulation of inflammatory gene expression has been at the forefront of studies of innate immunity and is coordinately regulated by transcription factors, including NF-κB, and chromatin modifiers. The growing evidence for involvement of chromatin in the regulation of gene expression in innate immune cells, has uncovered an evolutionarily conserved role of microbial sensing and chromatin remodeling. Toll-like receptors and RIG-I-like receptors trigger these signaling pathways leading to transcriptional expression of a set of genes involved in inflammation. Tightly regulated control of this gene expression is a paramount, and often foremost, goal of most biological endeavors. In this review, we will discuss the recent progress about the molecular mechanisms governing control of pro-inflammatory gene expression by an evolutionarily conserved novel nuclear protein Akirin2 in macrophages and its emergence as an essential link between NF-κB and chromatin remodelers for transcriptional regulation.
    Keywords macrophage ; innate immunity ; inflammation ; transcriptional regulation ; chromatin remodeling ; NF-κB ; Biology (General) ; QH301-705.5 ; Science ; Q
    Subject code 570 ; 571
    Language English
    Publishing date 2015-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Cutting Edge: Dysregulated CARD9 Signaling in Neutrophils Drives Inflammation in a Mouse Model of Neutrophilic Dermatoses.

    Tartey, Sarang / Gurung, Prajwal / Samir, Parimal / Burton, Amanda / Kanneganti, Thirumala-Devi

    Journal of immunology (Baltimore, Md. : 1950)

    2018  Volume 201, Issue 6, Page(s) 1639–1644

    Abstract: Mice homozygous for the Y208N amino acid substitution in the carboxy terminus of SHP-1 (referred to ... ...

    Abstract Mice homozygous for the Y208N amino acid substitution in the carboxy terminus of SHP-1 (referred to as
    MeSH term(s) Amino Acid Substitution ; Animals ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/immunology ; Dermatitis/genetics ; Dermatitis/immunology ; Dermatitis/pathology ; Disease Models, Animal ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Interleukin-1alpha/genetics ; Interleukin-1alpha/immunology ; Mice ; Mice, Knockout ; Mutation, Missense ; Neutrophils/immunology ; Neutrophils/pathology ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/immunology ; Receptors, Interleukin-1/genetics ; Receptors, Interleukin-1/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology
    Chemical Substances CARD Signaling Adaptor Proteins ; Card9 protein, mouse ; Interleukin-1alpha ; Receptors, Interleukin-1 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48) ; Ptpn6 protein, mouse (EC 3.1.3.48)
    Language English
    Publishing date 2018-08-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    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.1800760
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  10. Article ; Online: ASK1/2 signaling promotes inflammation in a mouse model of neutrophilic dermatosis.

    Tartey, Sarang / Gurung, Prajwal / Dasari, Tejasvi Krishna / Burton, Amanda / Kanneganti, Thirumala-Devi

    The Journal of clinical investigation

    2018  Volume 128, Issue 5, Page(s) 2042–2047

    Abstract: Mice homozygous for the Tyr208Asn amino acid substitution in the carboxy terminus of Src homology region 2 (SH2) domain-containing phosphatase 1 (SHP-1) (referred to as Ptpn6spin mice) spontaneously develop a severe inflammatory disease resembling ... ...

    Abstract Mice homozygous for the Tyr208Asn amino acid substitution in the carboxy terminus of Src homology region 2 (SH2) domain-containing phosphatase 1 (SHP-1) (referred to as Ptpn6spin mice) spontaneously develop a severe inflammatory disease resembling neutrophilic dermatosis in humans. Disease in Ptpn6spin mice is characterized by persistent footpad swelling and suppurative inflammation. Recently, in addition to IL-1α and IL-1R signaling, we demonstrated a pivotal role for several kinases such as SYK, RIPK1, and TAK1 in promoting inflammatory disease in Ptpn6spin mice. In order to identify new kinases involved in SHP-1-mediated inflammation, we took a genetic approach and discovered apoptosis signal-regulating kinases 1 and 2 (ASK1 and ASK2) as novel kinases regulating Ptpn6-mediated footpad inflammation. Double deletion of ASK1 and ASK2 abrogated cutaneous inflammatory disease in Ptpn6spin mice. This double deletion further rescued the splenomegaly and lymphomegaly caused by excessive neutrophil infiltration in Ptpn6spin mice. Mechanistically, ASK regulates Ptpn6spin-mediated disease by controlling proinflammatory signaling in the neutrophils. Collectively, the present study identifies SHP-1 and ASK signaling crosstalk as a critical regulator of IL-1α-driven inflammation and opens future avenues for finding novel drug targets to treat neutrophilic dermatosis in humans.
    MeSH term(s) Animals ; Disease Models, Animal ; Inflammation/enzymology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; MAP Kinase Kinase Kinase 5/genetics ; MAP Kinase Kinase Kinase 5/immunology ; MAP Kinase Kinase Kinase 5/metabolism ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/immunology ; MAP Kinase Kinase Kinases/metabolism ; Mice ; Mice, Knockout ; Neutrophil Infiltration ; Neutrophils/enzymology ; Neutrophils/immunology ; Neutrophils/pathology ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Sweet Syndrome/enzymology ; Sweet Syndrome/genetics ; Sweet Syndrome/immunology ; Sweet Syndrome/pathology
    Chemical Substances MAP Kinase Kinase Kinase 5 (EC 2.7.11.25) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 6 (EC 2.7.11.25) ; Map3k5 protein, mouse (EC 2.7.11.25) ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48) ; Ptpn6 protein, mouse (EC 3.1.3.48)
    Language English
    Publishing date 2018-04-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI98446
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