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  • The American Association of Immunologists  (19)
  • Medicine  (19)
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  • The American Association of Immunologists  (19)
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  • Medicine  (19)
RVK
  • 1
    Online Resource
    Online Resource
    E3 Ubiquitin Ligase RNF114 Inhibits Innate Immune Response to Red-Spotted Grouper Nervous Necrosis Virus Infection in Sea Perch by Targeting MAVS and TRAF3 to Mediate Their Degradation
    The American Association of Immunologists ; 2021
    In:  The Journal of Immunology Vol. 206, No. 1 ( 2021-01-01), p. 77-88
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 206, No. 1 ( 2021-01-01), p. 77-88
    Abstract: RIG-I–like receptor (RLR)–mediated antiviral signaling is critical to trigger the immune response to virus infection; however, the antiviral responses are also tightly regulated to avoid uncontrolled production of type I IFN by various mechanisms, including ubiquitination. In this study, an E3 ubiquitin ligase ring finger protein 114 (RNF114) from sea perch (Lateolabrax japonicus) (LjRNF114) was identified as a suppressor of RLR signaling pathways during red-spotted grouper nervous necrosis virus (RGNNV) infection. RGNNV infection promoted the expression of LjRNF114. Overexpression of LjRNF114 enhanced RGNNV replication, whereas knockdown of LjRNF114 led to opposite effects. Type I IFN production induced by RGNNV was suppressed by LjRNF114, which is dependent on its ubiquitin ligase activity. Moreover, LjRNF114 inhibited IFN promoter activation induced by key signaling molecules in RLR signaling pathways. We observed the interactions between LjRNF114 and both sea perch mitochondrial antiviral signaling protein (MAVS) and TNFR-associated factor 3 (TRAF3). Domain mapping experiments indicated that the RING and ubiquitin interacting motif domains of LjRNF114 were required for its interaction with TRAF3 and MAVS. We found that LjRNF114 targeted MAVS and TRAF3 for K27- and K48-linked ubiquitination and degradation, resulting in the inhibition of IFN production. Taken together, our study reveals, to our knowledge, a novel mechanism that LjRNF114 targets and promotes K27- and K48-linked ubiquitination of MAVS and TRAF3 to negatively regulate the RLR signaling pathways, promoting viral infection.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2000083
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2021
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    The Capsid Protein of Nervous Necrosis Virus Antagonizes Host Type I IFN Production by a Dual Strategy to Negatively Regulate Retinoic Acid–Inducible Gene-I–like Receptor Pathways
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 209, No. 2 ( 2022-07-15), p. 326-336
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 209, No. 2 ( 2022-07-15), p. 326-336
    Abstract: Nervous necrosis virus (NNV), a highly pathogenic RNA virus, is a major pathogen in the global aquaculture industry. To efficiently infect fish, NNV must evade or subvert the host IFN for their replication; however, the precise mechanisms remain to be elucidated. In this study, we reported that capsid protein (CP) of red-spotted grouper NNV (RGNNV) suppressed the IFN antiviral response to promote RGNNV replication in Lateolabrax japonicus brain cells, which depended on the ARM, S, and P domains of CP. CP showed an indirect or direct association with the key components of retinoic acid–inducible gene-I–like receptors signaling, L. japonicus TNFR-associated factor 3 (LjTRAF3) and IFN regulatory factor (LjIRF3), respectively, and degraded LjTRAF3 and LjIRF3 through the ubiquitin-proteasome pathway in HEK293T cells. Furthermore, we found that CP potentiated LjTRAF3 K48 ubiquitination degradation in a L. japonicus ring finger protein 114–dependent manner. LjIRF3 interacted with CP through the S domain of CP and the transcriptional activation domain or regulatory domain of LjIRF3. CP promoted LjIRF3 K48 ubiquitination degradation, leading to the reduced phosphorylation level and nuclear translocation of LjIRF3. Taken together, we demonstrated that CP inhibited type I IFN response by a dual strategy to potentiate the ubiquitination degradation of LjTRAF3 and LjIRF3. This study reveals a novel mechanism of RGNNV evading host immune response via its CP protein that will provide insights into the complex pathogenesis of NNV.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2100690
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    N Protein of Viral Hemorrhagic Septicemia Virus Suppresses STAT1-Mediated MHC Class II Transcription to Impair Antigen Presentation in Sea Perch, Lateolabrax japonicus
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 208, No. 5 ( 2022-03-01), p. 1076-1084
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 208, No. 5 ( 2022-03-01), p. 1076-1084
    Abstract: Upon virus invasion of the host, APCs process Ags to short peptides for presentation by MHC class II (MHC-II). The recognition of virus-derived peptides in the context of MHC-II by CD4+ T cells initiates the adaptive immune response for virus clearance. As a survival instinct, viruses have evolved mechanisms to evade Ag processing and presentation. In this study, we discovered that IFN-γ induced endogenous MHC-II expression by a sea perch brain cell line through the STAT1/IFN regulatory factor 1 (IRF1)/CIITA signaling pathway. Furthermore, viral hemorrhagic septicemia virus infection significantly inhibited the IFN-γ–induced expression of IRF1, CIITA, MHC-II-α, and MHC-II-β genes. By contrast, although STAT1 transcript was upregulated, paradoxically, the STAT1 protein level was attenuated. Moreover, overexpression analysis revealed that viral hemorrhagic septicemia virus N protein blocked the IFN-γ–induced expression of IRF1, CIITA, MHC-II-α, and MHC-II-β genes, but not the STAT1 gene. We also found out that N protein interacted with STAT1 and enhanced the overall ubiquitination level of proteins, including STAT1 in Lateolabrax japonicus brain cells. Enhanced ubiquitination of STAT1 through K48-linked ubiquitination led to its degradation through the ubiquitin–proteasome pathway, thereby inhibiting the biological function of STAT1. Our study suggests that aquatic viruses target Ag presentation in lower vertebrates for immune evasion as do mammalian viruses.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2100939
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
    Online Resource
    Intestinal Epithelial TLR-4 Activation Is Required for the Development of Acute Lung Injury after Trauma/Hemorrhagic Shock via the Release of HMGB1 from the Gut
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 10 ( 2015-05-15), p. 4931-4939
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 10 ( 2015-05-15), p. 4931-4939
    Abstract: The mechanisms that lead to the development of remote lung injury after trauma remain unknown, although a central role for the gut in the induction of lung injury has been postulated. We hypothesized that the development of remote lung injury after trauma/hemorrhagic shock requires activation of TLR4 in the intestinal epithelium, and we sought to determine the mechanisms involved. We show that trauma/hemorrhagic shock caused lung injury in wild-type mice, but not in mice that lack TLR4 in the intestinal epithelium, confirming the importance of intestinal TLR4 activation in the process. Activation of intestinal TLR4 after trauma led to increased endoplasmic reticulum (ER) stress, enterocyte apoptosis, and the release of circulating HMGB1, whereas inhibition of ER stress attenuated apoptosis, reduced circulating HMGB1, and decreased lung injury severity. Neutralization of circulating HMGB1 led to reduced severity of lung injury after trauma, and mice that lack HMGB1 in the intestinal epithelium were protected from the development of lung injury, confirming the importance of the intestine as the source of HMGB1, whose release of HMGB1 induced a rapid protein kinase C ζ–mediated internalization of surface tight junctions in the pulmonary epithelium. Strikingly, the use of a novel small-molecule TLR4 inhibitor reduced intestinal ER stress, decreased circulating HMGB1, and preserved lung architecture after trauma. Thus, intestinal epithelial TLR4 activation leads to HMGB1 release from the gut and the development of lung injury, whereas strategies that block upstream TLR4 signaling may offer pulmonary protective strategies after trauma.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1402490
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    In Vivo Inhibition of Type I Interferon Transcription in Genital HSV-2 Lesions (134.72)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 134.72-134.72
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 134.72-134.72
    Abstract: We performed transcriptional analysis and immunocytochemistry (ICC) of sequential biopsies of lesional tissue of immunocompetent persons with recurrent HSV-2 infection. Histologic analysis of these biopsies indicated a massive infiltration of monocytes/macrophages along with a large amount of myeloid and a small number of plasmacytoid dendritic cells in the dermis of these lesional biopsies. IFNB1 and IFN-α were weakly expressed and IFNG potently induced during time periods in which there was abundant detection of HSV-2 antigens and gene expression. Transcriptional arrays of the same anatomic area over time (newly healed, 2 and 4 weeks post healing) in which no HSV DNA/RNA or antigen was detected continued to show that IFNB1 and IFN-α were barely detectable. IFNG persisted in lesional tissue, albeit at lower levels as compared with active lesions. Interferon-stimulated genes (ISGs) were also markedly up-regulated with expression patterns more clearly resembling those in primary human fibroblasts treated by IFNG than by IFNB1. The presence of a very large number of innate cells capable of sensing HSV-2 infection and synthesizing type I IFN by both histologic and transcriptional analyses associated with extremely low levels of IFN-α and IFNB1 even in the earliest lesional biopsies suggests a potent alteration in host defense during HSV-2 infection in vivo. This block of type I IFN by HSV-2 may be a major factor in allowing the virus to breakthrough host mucosal defenses.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.182.Supp.134.72
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Regulation of Anion Channel LRRC8 Volume-Regulated Anion Channels in Transport of 2′3′-Cyclic GMP–AMP and Cisplatin under Steady State and Inflammation
    The American Association of Immunologists ; 2021
    In:  The Journal of Immunology Vol. 206, No. 9 ( 2021-05-01), p. 2061-2074
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 206, No. 9 ( 2021-05-01), p. 2061-2074
    Abstract: The recently identified anion channel LRRC8 volume-regulated anion channels (VRACs) are heteromeric hexamers constituted with the obligate LRRC8A subunit paired with at least one of the accessory LRRC8B to LRRC8E subunits. In addition to transport chloride, taurine, and glutamate, LRRC8 VRACs also transport the anticancer agent cisplatin and STING agonists 2′3′-cyclic GMP–AMP (cGAMP) and cyclic dinucleotides; hence, they are implicated in a variety of physiological and pathological processes, such as cell swelling, stroke, cancer, and viral infection. Although the subunit composition largely determines VRAC substrate specificity, the opening of various VRAC pores under physiological and pathological settings remains enigmatic. In this study, we demonstrated that VRACs comprising LRRC8A and LRRC8E (LRRC8A/E–containing VRACs), specialized in cGAMP transport, can be opened by a protein component present in serum under resting condition. Serum depletion ablated the tonic activity of LRRC8A/E–containing VRACs, decreasing cGAMP transport in various human and murine cells. Also, heating or proteinase K treatment abolished the ability of serum to activate VRAC. Genetic analyses revealed a crucial role for cGAMP synthase (cGAS) in serum/TNF–promoted VRAC activation. Notably, the presence of cGAS on the plasma membrane, rather than its DNA-binding or enzymatic activity, enabled VRAC activation. Moreover, phospholipid PIP2 seemed to be instrumental in the membrane localization of cGAS and its association with VRACs. Corroborating a role for LRRC8A/D–containing VRACs in cisplatin transport, serum and TNF markedly potentiated cisplatin uptake and killing of cancer cells derived from human or mouse. Together, these observations provide new insights into the complex regulation of VRAC activation and suggest a novel approach to enhance the efficacy of cGAMP and cisplatin in treating infection and cancer.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2000989
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2021
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    Duck Tembusu Virus Nonstructural Protein 1 Antagonizes IFN-β Signaling Pathways by Targeting VISA
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 197, No. 12 ( 2016-12-15), p. 4704-4713
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 197, No. 12 ( 2016-12-15), p. 4704-4713
    Abstract: Duck Tembusu virus (DTMUV) is an emergent infectious pathogen that has caused severe disease in ducks and huge economic losses to the poultry industry in China since 2009. Previously, we showed that DTMUV inhibits IFN-β induction early in infection; however, the mechanisms of the inhibition of innate immune responses remain poorly understood. In this study, we screened DTMUV-encoded structural and nonstructural proteins using reporter assays and found that DTMUV NS1 markedly suppressed virus-triggered IFN-β expression by inhibiting retinoic acid–inducible gene I–like receptor signaling. Moreover, we found that DTMUV NS1 specifically interacted with the C-terminal domain of virus-induced signaling adaptor and impaired the association of retinoic acid–inducible gene I or melanoma differentiation-associated gene 5 and virus-induced signaling adaptor, thereby downregulating the retinoic acid–inducible gene I–like receptor–mediated signal transduction and cellular antiviral responses, leading to evasion of the innate immune response. Together, our findings reveal a novel mechanism manipulated by DTMUV to circumvent the host antiviral immune response.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1502317
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 8
    Online Resource
    Online Resource
    Tissue resident memory CD8 T cells augment innate immunity for tissue-wide antiviral protection
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 196, No. 1_Supplement ( 2016-05-01), p. 148.7-148.7
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 196, No. 1_Supplement ( 2016-05-01), p. 148.7-148.7
    Abstract: Tissue-resident memory (TRM) CD8+ T cells provide effective, localized protection against pathogen re-encountering at barrier surfaces. During human herpes simplex virus 2 (HSV-2) infection, TRM CD8+ T cells persist at dermal-epidermal junction, interacting with basal keratinocytes and performing immune containment. The precise mechanism of how a few TRM CD8+ T cells convey broad tissue-wide protection is unclear. This study investigated the effects of TRM CD8+ T cells on tissue microenvironment by laser microdissecting and transcription profiling keratinocytes during human genital HSV-2 infection. In asymptomatic reactivation and lesion forming recurrences, keratinocytes exhibited a cell-intrinsic antiviral signature. Genes involved in RNA trafficking and protein translation were down-regulated, while a subset of interferon stimulated genes (ISGs) was elevated. The ISG expression was widely spread throughout the epidermis in the affected area. IFN-γ was expressed in TRM CD8+ T cells, but IFN-α and IFN-β were undetectable in keratinocytes and whole tissue. In primary cultured keratinocyte and fibroblast cells, pretreatment of IFN-γ delayed and restricted HSV gene expression at immediate-early stage of viral transcription. The inhibition on viral gene expression was dose-dependent and relied on IFN-γ receptor signaling. Thus, by harnessing cell-intrinsic innate immunity, TRM CD8+ T cells convey a tissue-wide antiviral protection in a non-cytolytic manner.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.196.Supp.148.7
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 9
    Online Resource
    Online Resource
    Cytolytic Potentials of CD8+ T Cells Persisting in Genital Skin and Mucosa after HSV-2 Reactivation (45.16)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 45.16-45.16
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 45.16-45.16
    Abstract: We have previously demonstrated that CD8+ T cells, including HSV-2 specific CD8+ T cells, persisted in genital skin for months after the herpes lesion completely healed, and preferentially accumulated at the dermal-epidermal junction where sensory nerve endings were enriched. These persisting CD8+ T cells have been postulated in the containment of the reactivating virus before clinical symptomatic lesion occurs. To understand functions of persisting CD8+ T cells in human, we have combined immunofluorescent (IF) staining, laser capture microdissection (LCM) and RT-PCR to analyze the gene expression of CD8+ T cells at the dermal-epidermal junction in post-healed lesion biopsy. CD8+ T cells were captured at a single cell level. The purity was validated by the lack of CD4 and a 100-fold more enriched CD8 expression in LCM captured cells than in whole tissue sections. In captured CD8+ T cells, we detected up-regulation of genes encoding cytolytic granules, such as perforin and granzyme B, as compared to keratinocytes in the epidermis. The expression of cytolytic granules was further confirmed by IF staining of persistent CD8+ T cells, even in post-healed biopsy of acyclovir treated individual. Our data strongly indicated the cytolytic potentials of CD8+ T cells persisting at the dermal-epidermal junction and implicated their role in immune surveillance against HSV-2 reactivation in skin and mucosa. This work was supported by NIH grants R37 AI042528 and PO1 AI030731.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.182.Supp.45.16
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 10
    Online Resource
    Online Resource
    Histone Demethylase Jmjd3 Controls T-Cell Trafficking and Persistence by Interacting with Klf2 for Expression of Pdlim4
    The American Association of Immunologists ; 2018
    In:  The Journal of Immunology Vol. 200, No. 1_Supplement ( 2018-05-01), p. 102.21-102.21
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 200, No. 1_Supplement ( 2018-05-01), p. 102.21-102.21
    Abstract: Jmjd3, a histone H3K27 demethylase, plays a critical role in gene expression and T-cell differentiation, but its role and mechanisms in T cell trafficking remain poorly understood. Here we have shown that Jmjd3 deficiency in CD4+ T cells resulted in the accumulation of T cells in the thymus, but a reduced number in secondary lymphoid organs. To understand the molecular mechanisms of Jmjd3 action, we identified PDLIM4 as a significantly downregulated target gene in Jmjd3-deficient CD4+ T cells by gene profiling and ChIP-seq analyses. Further investigation shows that Jmjd3 bound to the promoter and gene body regions of PDLIM4 gene and regulated PDLIM4 expression by interacting with zinc finger transcription factor KLF2. Furthermore, we showed that PDLIM4 was involved in filamentous actin (F-actin) remodeling, thus functioning as a key regulator of T cell trafficking. Our findings have identified PDLIM4 as a novel Jmjd3 target gene that affects T-cell trafficking, and provided insights into the molecular mechanisms by which Jmjd3 regulates genes participate in T-cell trafficking.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.200.Supp.102.21
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2018
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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