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Journal of Immunology
Journal Prestige (SJR): 2.837
Citation Impact (citeScore): 5
Number of Followers: 71  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 0022-1767 - ISSN (Online) 1550-6606
Published by American Assoc of Immunologists Homepage  [2 journals]
  • Top Reads [TOP READS]

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      Pages: 2193 - 2193
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2190019
      Issue No: Vol. 207, No. 9 (2021)
       
  • SysInflam HuDB, a Web Resource for Mining Human Blood Cells Transcriptomic
           Data Associated with Systemic Inflammatory Responses to Sepsis [IMMUNOLOGY
           NOTES AND RESOURCES]

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      Authors: Toufiq, M; Huang, S. S. Y, Boughorbel, S, Alfaki, M, Rinchai, D, Saraiva, L. R, Chaussabel, D, Garand, M.
      Pages: 2195 - 2202
      Abstract: Sepsis develops after a dysregulated host inflammatory response to a systemic infection. Identification of sepsis biomarkers has been challenging because of the multifactorial causes of disease susceptibility and progression. Public transcriptomic data are a valuable resource for mechanistic discoveries and cross-studies concordance of heterogeneous diseases. Nonetheless, the approach requires structured methodologies and effective visualization tools for meaningful data interpretation. Currently, no such database exists for sepsis or systemic inflammatory diseases in human. Hence we curated SysInflam HuDB (http://sepsis.gxbsidra.org/dm3/geneBrowser/list), a unique collection of human blood transcriptomic datasets associated with systemic inflammatory responses to sepsis. The transcriptome collection and the associated clinical metadata are integrated onto a user-friendly and Web-based interface that allows the simultaneous exploration, visualization, and interpretation of multiple datasets stemming from different study designs. To date, the collection encompasses 62 datasets and 5719 individual profiles. Concordance of gene expression changes with the associated literature was assessed, and additional analyses are presented to showcase database utility. Combined with custom data visualization at the group and individual levels, SysInflam HuDB facilitates the identification of specific human blood gene signatures in response to infection (e.g., patients with sepsis versus healthy control subjects) and the delineation of major genetic drivers associated with inflammation onset and progression under various conditions.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100697
      Issue No: Vol. 207, No. 9 (2021)
       
  • More Than Two to Tango: Mesenchymal Cells Are Required for Early T Cell
           Development [PILLARS OF IMMUNOLOGY]

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      Authors: Anderson M. K.
      Pages: 2203 - 2204
      Abstract: This Pillars of Immunology article is a commentary on "MHC class II-positive epithelium and mesenchyme cells are both required for T-cell development in the thymus," a pivotal article written by G. Anderson, E. J. Jenkinson, N. C. Moore, and J. J. Owen, and published in Nature, in 1993 https://www.nature.com/articles/362070a0.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100677
      Issue No: Vol. 207, No. 9 (2021)
       
  • IL-10 as a Th2 Cytokine: Differences Between Mice and Humans [BRIEF
           REVIEWS]

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      Authors: Rasquinha, M. T; Sur, M, Lasrado, N, Reddy, J.
      Pages: 2205 - 2215
      Abstract: The discovery of IL-10 more than 30 years ago marked the beginning of our understanding of how cytokines regulate immune responses, based on cross-regulation between Th1 and Th2 cytokines. Although multiple cell types were shown to produce IL-10, its identity as a Th2 cytokine remained strong because it was rigidly associated with Th2 clones in mice, whereas both Th1 and Th2 clones could secrete IL-10 in humans. However, as new Th1/Th2 cell functionalities emerged, anti-inflammatory action of IL-10 gained more attention than its inhibitory effect on Th1 cells, which may occur as an indirect consequence of suppression of APCs. This notion is also supported by the discovery of regulatory T cells, whose suppressor functions involve the mediation of IL-10, among other molecules. From this perspective, we discuss the functionalities of IL-10 by highlighting important differences between mice and humans with an emphasis on the Th1 and Th2 paradigm.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100565
      Issue No: Vol. 207, No. 9 (2021)
       
  • Cutting Edge: A Threshold of B Cell Costimulatory Signals Is Required for
           Spontaneous Germinal Center Formation in Autoimmunity [CUTTING EDGE]

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      Authors: Chiang, K; Largent, A. D, Arkatkar, T, Thouvenel, C. D, Du, S. W, Shumlak, N, Woods, J, Li, Q.-Z, Liu, Y, Hou, B, Rawlings, D. J, Jackson, S. W.
      Pages: 2217 - 2222
      Abstract: Key Points
      B cell–derived costimulation facilitates autoimmune GC formation.
      Extrafollicular activation and GCs contribute to lupus autoantibodies.
      Age-associated B cells develop via a GC-independent extrafollicular pathway.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100548
      Issue No: Vol. 207, No. 9 (2021)
       
  • The Loss of H3K27 Histone Demethylase Utx in T Cells Aggravates Allergic
           Contact Dermatitis [ALLERGY AND OTHER HYPERSENSITIVITIES]

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      Authors: Inoue, T; Omori-Miyake, M, Maruyama, S, Okabe, M, Kuwahara, M, Honda, H, Miura, H, Yamashita, M.
      Pages: 2223 - 2234
      Abstract: Key Points
      Utx and Jmjd3 play distinct roles in the development of allergic contact dermatitis.
      Utx-deficient T cells enhance the accumulation of myeloid cells in the lesional skin.
      Utx deficiency decreases the ratio of regulatory T cells to conventional CD4+ T cells.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2001160
      Issue No: Vol. 207, No. 9 (2021)
       
  • ERAP1 Controls the Autoimmune Response against Melanocytes in Psoriasis by
           Generating the Melanocyte Autoantigen and Regulating Its Amount for
           HLA-C*06:02 Presentation [AUTOIMMUNITY]

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      Authors: Arakawa, A; Reeves, E, Vollmer, S, Arakawa, Y, He, M, Galinski, A, Stöhr, J, Dornmair, K, James, E, Prinz, J. C.
      Pages: 2235 - 2244
      Abstract: Key Points
      ERAP1 generates the autoantigen for presentation by HLA-C*06:02 in psoriasis.
      ERAP1 haplotypes control the autoimmune response by different autoantigen yields.
      HLA-C–restricted immune responses may be particularly dependent on ERAP1 function.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100686
      Issue No: Vol. 207, No. 9 (2021)
       
  • Regulation and Role of {alpha}E Integrin and Gut Homing Integrins in
           Migration and Retention of Intestinal Lymphocytes during Inflammatory
           Bowel Disease [CLINICAL AND HUMAN IMMUNOLOGY]

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      Authors: Keir, M. E; Fuh, F, Ichikawa, R, Acres, M, Hackney, J. A, Hulme, G, Carey, C. D, Palmer, J, Jones, C. J, Long, A. K, Jiang, J, Klabunde, S, Mansfield, J. C, Looney, C. M, Faubion, W. A, Filby, A, Kirby, J. A, McBride, J, Lamb, C. A.
      Pages: 2245 - 2254
      Abstract: Key Points
      Adhesion molecules are upregulated in inflamed intestinal mucosa in IBD patients.
      Baseline β7 expression does not impact αE induction or gene expression in T cells.
      Phospho-SMAD3 is increased in inflamed mucosa in IBD.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100220
      Issue No: Vol. 207, No. 9 (2021)
       
  • MHC Class II Ubiquitination Regulates Dendritic Cell Function and Immunity
           [IMMUNE REGULATION]

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      Authors: Wilson, K. R; Jenika, D, Blum, A. B, Macri, C, Xu, B, Liu, H, Schriek, P, Schienstock, D, Francis, L, Makota, F. V, Ishido, S, Mueller, S. N, Lahoud, M. H, Caminschi, I, Edgington-Mitchell, L. E, Villadangos, J. A, Mintern, J. D.
      Pages: 2255 - 2264
      Abstract: Key Points
      MHC II ubiquitination impacts dendritic cell numbers and phenotype.
      MHC II ubiquitination is critical for Ag-dependent T cell responses in vivo.
      MHC II ubiquitination is required for Ab responses.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2001426
      Issue No: Vol. 207, No. 9 (2021)
       
  • Down Syndrome Cell Adhesion Molecule Triggers Membrane-to-Nucleus
           Signaling-Regulated Hemocyte Proliferation against Bacterial Infection in
           Invertebrates [IMMUNE REGULATION]

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      Authors: Li, H; Jin, X.-K, Zhou, K.-M, Zhao, H, Zhao, Y.-H, Wang, Q, Li, W.-W.
      Pages: 2265 - 2277
      Abstract: Key Points
      Protease ADAM10 cleaves the ectodomain of Dscam upon bacterial infection.
      IPO5 binds and translocates Dscam intracellular domains from cytoplasm into nuclei.
      Nuclear imported Dscam regulates hemocytes proliferation.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100575
      Issue No: Vol. 207, No. 9 (2021)
       
  • Exposure to Systemic Immunosuppressive Ultraviolet Radiation Alters T Cell
           Recirculation through Sphingosine-1-Phosphate [IMMUNE REGULATION]

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      Authors: Tse, B. C. Y; Ireland, R. A, Lee, J. Y, Marsh-Wakefield, F, Kok, L. F, Don, A. S, Byrne, S. N.
      Pages: 2278 - 2287
      Abstract: Systemic suppression of adaptive immune responses is a major way in which UV radiation contributes to skin cancer development. Immune suppression is also likely to explain how UV protects from some autoimmune diseases, such as multiple sclerosis. However, the mechanisms underlying UV-mediated systemic immune suppression are not well understood. Exposure of C57BL/6 mice to doses of UV known to suppress systemic autoimmunity led to the accumulation of cells within the skin-draining lymph nodes and away from non–skin-draining lymph nodes. Transfer of CD45.1+ cells from nonirradiated donors into CD45.2+ UV-irradiated recipients resulted in preferential accumulation of donor naive T cells and a decrease in activated T cells within skin-draining lymph nodes. A single dose of immune-suppressive UV was all that was required to cause a redistribution of naive and central memory T cells from peripheral blood to the skin-draining lymph nodes. Specifically, CD69-independent increases in sphingosine-1-phosphate (S1P) receptor 1–negative naive and central memory T cells occurred in these lymph nodes. Mass spectrometry analysis showed UV-mediated activation of sphingosine kinase 1 activity, resulting in an increase in S1P levels within the lymph nodes. Topical application of a sphingosine kinase inhibitor on the skin prior to UV irradiation eliminated the UV-induced increase in lymph node S1P and T cell numbers. Thus, exposure to immunosuppressive UV disrupts T cell recirculation by manipulating the S1P pathway.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2001261
      Issue No: Vol. 207, No. 9 (2021)
       
  • Signal Integration by Translocation and Phosphorylation of PKC{delta} in
           the B Cell Alternate Pathway [IMMUNE REGULATION]

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      Authors: Khan, N; Hu, Y, Lowell, C. A, Rothstein, T. L.
      Pages: 2288 - 2296
      Abstract: Key Points
      IL-4 treatment induces a signalosome-independent alternate pathway for BCR signaling.
      Lyn is autophosphorylated after IL-4 treatment in membranes.
      PKC is translocated and phosphorylated by Lyn in membranes through the alternate pathway.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100295
      Issue No: Vol. 207, No. 9 (2021)
       
  • Sec22b Regulates Inflammatory Responses by Controlling the Nuclear
           Translocation of NF-{kappa}B and the Secretion of Inflammatory Mediators
           [INNATE IMMUNITY AND INFLAMMATION]

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      Authors: Arango Duque, G; Dion, R, Matte, C, Fabie, A, Descoteaux, J, Stäger, S, Descoteaux, A.
      Pages: 2297 - 2309
      Abstract: Key Points
      iNOS is an ERGIC/Golgi protein that traffics to the surface of the phagolysosome.
      The SNARE Sec22b indirectly controls the secretion of NO, TNF, and IL-6.
      Sec22b mediates NF-B translocation thereby regulating iNOS and cytokine expression.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100258
      Issue No: Vol. 207, No. 9 (2021)
       
  • TLR-4 Agonist Induces IFN-{gamma} Production Selectively in
           Proinflammatory Human M1 Macrophages through the PI3K-mTOR- and
           JNK-MAPK-Activated p70S6K Pathway [INNATE IMMUNITY AND INFLAMMATION]

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      Authors: Gajanayaka, N; Dong, S. X. M, Ali, H, Iqbal, S, Mookerjee, A, Lawton, D. A, Caballero, R. E, Cassol, E, Cameron, D. W, Angel, J. B, Crawley, A. M, Kumar, A.
      Pages: 2310 - 2324
      Abstract: IFN-, a proinflammatory cytokine produced primarily by T cells and NK cells, activates macrophages and engages mechanisms to control pathogens. Although there is evidence of IFN- production by murine macrophages, IFN- production by normal human macrophages and their subsets remains unknown. Herein, we show that human M1 macrophages generated by IFN- and IL-12– and IL-18–stimulated monocyte-derived macrophages (M0) produce significant levels of IFN-. Further stimulation of IL-12/IL-18–primed macrophages or M1 macrophages with agonists for TLR-2, TLR-3, or TLR-4 significantly enhanced IFN- production in contrast to the similarly stimulated M0, M2a, M2b, and M2c macrophages. Similarly, M1 macrophages generated from COVID-19–infected patients’ macrophages produced IFN- that was enhanced following LPS stimulation. The inhibition of M1 differentiation by Jak inhibitors reversed LPS-induced IFN- production, suggesting that differentiation with IFN- plays a key role in IFN- induction. We subsequently investigated the signaling pathway(s) responsible for TLR-4–induced IFN- production in M1 macrophages. Our results show that TLR-4–induced IFN- production is regulated by the ribosomal protein S6 kinase (p70S6K) through the activation of PI3K, the mammalian target of rapamycin complex 1/2 (mTORC1/2), and the JNK MAPK pathways. These results suggest that M1-derived IFN- may play a key role in inflammation that may be augmented following bacterial/viral infections. Moreover, blocking the mTORC1/2, PI3K, and JNK MAPKs in macrophages may be of potential translational significance in preventing macrophage-mediated inflammatory diseases.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2001191
      Issue No: Vol. 207, No. 9 (2021)
       
  • Dendritic Cell-Specific Role for Pellino2 as a Mediator of TLR9 Signaling
           Pathway [INNATE IMMUNITY AND INFLAMMATION]

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      Authors: Oleszycka, E; Rodgers, A. M, Xu, L, Moynagh, P. N.
      Pages: 2325 - 2336
      Abstract: Ubiquitination regulates immune signaling, and multiple E3 ubiquitin ligases have been studied in the context of their role in immunity. Despite this progress, the physiological roles of the Pellino E3 ubiquitin ligases, especially Pellino2, in immune regulation remain largely unknown. Accordingly, this study aimed to elucidate the role of Pellino2 in murine dendritic cells (DCs). In this study, we reveal a critical role of Pellino2 in regulation of the proinflammatory response following TLR9 stimulation. Pellino2-deficient murine DCs show impaired secretion of IL-6 and IL-12. Loss of Pellino2 does not affect TLR9-induced activation of NF-B or MAPKs, pathways that drive expression of IL-6 and IL-12. Furthermore, DCs from Pellino2-deficient mice show impaired production of type I IFN following endosomal TLR9 activation, and it partly mediates a feed-forward loop of IFN-β that promotes IL-12 production in DCs. We also observe that Pellino2 in murine DCs is downregulated following TLR9 stimulation, and its overexpression induces upregulation of both IFN-β and IL-12, demonstrating the sufficiency of Pellino2 in driving these responses. This suggests that Pellino2 is critical for executing TLR9 signaling, with its expression being tightly regulated to prevent excessive inflammatory response. Overall, this study highlights a (to our knowledge) novel role for Pellino2 in regulating DC functions and further supports important roles for Pellino proteins in mediating and controlling immunity.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100236
      Issue No: Vol. 207, No. 9 (2021)
       
  • Overexpression of Transmembrane TNF Drives Development of Ectopic Lymphoid
           Structures in the Bone Marrow and B Cell Lineage Alterations in
           Experimental Spondyloarthritis [INNATE IMMUNITY AND INFLAMMATION]

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      Authors: Kaaij, M. H; Rip, J, Jeucken, K. C. M, Kan, Y. Y, van Rooijen, C. C. N, Saris, J, Pots, D, Frey, S, Grootjans, J, Schett, G, van Duivenvoorde, L. M, Nolte, M. A, Hendriks, R. W, Corneth, O. B. J, van Hamburg, J. P, Baeten, D. L. P, Tas, S. W.
      Pages: 2337 - 2346
      Abstract: Key Points
      tmTNF overexpression causes formation of ELS.
      ELS are located in BM next to inflammatory joint and spine lesions.
      ELS formation is accompanied by increased IgA class switching.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100512
      Issue No: Vol. 207, No. 9 (2021)
       
  • Downregulation of Perilipin1 by the Immune Deficiency Pathway Leads to
           Lipid Droplet Reconfiguration and Adaptation to Bacterial Infection in
           Drosophila [INNATE IMMUNITY AND INFLAMMATION]

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      Authors: Wang, L; Lin, J, Yu, J, Yang, K, Sun, L, Tang, H, Pan, L.
      Pages: 2347 - 2358
      Abstract: Key Points
      LDs of Drosophila fat body become bigger in response to IMD signaling activation.
      IMD signaling suppresses perilipin1 expression, which promotes LDs’ growth.
      Enlarged LDs benefit flies against bacterial infection via an antioxidative role.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100343
      Issue No: Vol. 207, No. 9 (2021)
       
  • Selective Induction of Cell Death in Human M1 Macrophages by Smac Mimetics
           Is Mediated by cIAP-2 and RIPK-1/3 through the Activation of mTORC [INNATE
           IMMUNITY AND INFLAMMATION]

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      Authors: Ali, H; Dong, S. X. M, Gajanayaka, N, Cassol, E, Angel, J. B, Kumar, A.
      Pages: 2359 - 2373
      Abstract: Key Points
      Human M1 macrophages are highly susceptible to SM-induced cell death.
      This cell death is mediated by cIAP-2 and RIPK-1/3 degradation via mTOR activation.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100108
      Issue No: Vol. 207, No. 9 (2021)
       
  • Lymphocyte Activation Gene-3 Regulates Dendritic Cell Metabolic Programing
           and T Cell Priming Function [INNATE IMMUNITY AND INFLAMMATION]

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      Authors: Garcia Cruz, D; Giri, R. R, Gamiotea Turro, D, Balsbaugh, J. L, Adler, A. J, Rodriguez, A.
      Pages: 2374 - 2384
      Abstract: Key Points
      LAG3 deficiency in dendritic cells is associated with increased glycolysis.
      LAG3 deficiency in dendritic cells enhances naive T cell priming.
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2001188
      Issue No: Vol. 207, No. 9 (2021)
       
  • Correction: Engineered Pigs Carrying a Gain-of-Function NLRP3 Homozygous
           Mutation Can Survive to Adulthood and Accurately Recapitulate Human
           Systemic Spontaneous Inflammatory Responses [CORRECTIONS]

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      Authors: Li, W; Shi, L, Zhuang, Z, Wu, H, Lian, M, Chen, Y, Li, L, Ge, W, Jin, Q, Zhang, Q, Zhao, Y, Liu, Z, Ouyang, Z, Ye, Y, Li, Y, Wang, H, Liao, Y, Quan, L, Xiao, L, Lai, L, Meng, G, Wang, K.
      Pages: 2385 - 2386
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100753
      Issue No: Vol. 207, No. 9 (2021)
       
  • Correction: Kavain Reduces Porphyromonas gingivalis-Induced Adipocyte
           Inflammation: Role of PGC-1{alpha} Signaling [CORRECTIONS]

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      Authors: Singh, S. P; Huck, O, Abraham, N. G, Amar, S.
      Pages: 2387 - 2387
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100846
      Issue No: Vol. 207, No. 9 (2021)
       
  • Correction: Control of Allergen-Induced Inflammation and
           Hyperresponsiveness by the Metalloproteinase ADAMTS-12 [CORRECTIONS]

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      Authors: Paulissen, G; El Hour, M, Rocks, N, Gueders, M. M, Bureau, F, Foidart, J.-M, Lopez-Otin, C, Noel, A, Cataldo, D. D.
      Pages: 2388 - 2389
      PubDate: 2021-10-18T13:00:24-07:00
      DOI: 10.4049/jimmunol.2100809
      Issue No: Vol. 207, No. 9 (2021)
       
 
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