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J Immunol (2019) 203 (4): 773–774.


J Immunol (2019) 203 (4): 775–781.


J Immunol (2019) 203 (4): 783–788.

  • TAK1 protects macrophages from proinflammatory cell death in TLR and TNFRI signaling.

  • The cell death machinery is dependent on active caspases and GSDMD processing.

  • TAK1 in macrophages both positively and negatively controls host inflammatory responses.

J Immunol (2019) 203 (4): 789–794.

  • A bicistronic dual-reporter mouse enables visualization of allelic CXCR3 expression.

  • CXCR3 escapes X chromosome inactivation (XCI) in T cells in vivo during infection.

  • XCI escape by CXCR3 potentially contributes to enhanced Th1 responses in females.

J Immunol (2019) 203 (4): 795–800.

  • Citrullination in macrophages is induced during pyroptosis.

  • The NLRP3 inflammasome is regulated by Ca2+-dependent PAD enzymes.

J Immunol (2019) 203 (4): 801–806.

  • Tcf1-mediated repression of Blimp1 is functionally critical for TFH differentiation.

  • An intron-3 regulatory region in the Blimp1 gene is necessary for optimal TFH response.

J Immunol (2019) 203 (4): 807–812.

  • BCG immunization alters the cell types targeted for early M. tuberculosis infection.

  • Vaccine-induced CD4 T cells are required for this transfer of infection.

  • T cell activation within the lung first occurs distal to sites of infection.


J Immunol (2019) 203 (4): 813–824.

  • Lone star tick proteins induce IgE production and hypersensitivity reactions in mice.

  • CD4+ T cell help is required for both sensitization and recall IgE production.

  • MyD88 deficiency in B cells disrupts IgE production.


J Immunol (2019) 203 (4): 825–834.

  • Injection of allogeneic Ag-loaded EVs significantly increases IgG in mice.

  • Two injections of syngeneic or allogeneic EVs result in long-term immunity.

  • Syngeneic and allogeneic EVs are equally potent in inhibiting tumor growth.


J Immunol (2019) 203 (4): 835–843.

  • We studied whether and to what extent IFN-α causes SLE.

  • We found that increase of IFN-α alone was sufficient to cause SLE.

  • The DNT cells as expanded by IFN-α directly caused organ manifestation of SLE.

J Immunol (2019) 203 (4): 844–852.

  • PD-1 blockade or deficiency unleashes follicular insulin-specific CD4+ T and B cells.

  • PD-1 limits T follicular helper cell survival in the germinal center.

  • PD-1 blockade increases insulin autoantibody production in diabetes-prone mice.


J Immunol (2019) 203 (4): 853–863.

  • Cholesterol crystals induce coagulation through monocyte TF.

  • Monocyte TF induction is blocked by complement inhibitors to C3, C5, or C5aR1.

  • Monocyte TF induction is dependent on complement C5aR1.


J Immunol (2019) 203 (4): 864–872.

  • COX-1 deficiency impaired TFH cell development during influenza infection and KLH immunization.

  • COX-1–derived metabolite PGE2 and its receptors EP2/EP4 mediate the effect of COX-1 on TFH cells.

J Immunol (2019) 203 (4): 873–880.

  • TRIM29 is induced in NK cells and inhibits NK functions.

  • TRIM29 deletion in NK cells enhances IFN-γ production.

  • TRIM29 ubiquitinates and degrades TAB2 in activated NK cells.


J Immunol (2019) 203 (4): 881–887.

  • In vivo administration of a peptide can promote T cell selection in the thymus.

  • Affinity for TCR/pMHC during positive selection fine-tunes peripheral T cells.


J Immunol (2019) 203 (4): 888–898.

  • MS-associated SNP rs17066096 influences IL-22BP levels.

  • IL-22BP promotes neuroinflammation by blocking IL-22 signaling.

  • IL-22 reduces T cell IFN-γ production.


J Immunol (2019) 203 (4): 899–910.

  • KMO inhibition improved clinical outcomes of CD4+ T cell counts and body weight.

  • KMO inhibition increased naive T cell frequency and lowered PD-1 expression.


J Immunol (2019) 203 (4): 911–921.

  • TLR ligands induce IL-26 secretion from PBMCs in an IL-1β–dependent manner.

  • IL-1β induces rapid IL-26 release by IL-1RI+ Th17 cells without TCR activation.

  • IL-1β–stimulated T cells mediate an antimicrobial activity via IL-26.

J Immunol (2019) 203 (4): 922–935.

  • IL-36γ conferred MDMs M. tuberculosis resistance through activation of autophagy.

  • IL-36γ induced autophagy relying on WNT5A/COX-2/AKT/mTOR axis.

  • IL-36γ may be a potential candidate for immune therapy of tuberculosis.

J Immunol (2019) 203 (4): 936–945.

  • Low affinity–stimulated CD8+ T cells have an advantage in forming TRM.

  • High and low affinity–stimulated TRM have distinct transcriptomes.

  • TRM longevity is not impacted by strength of TCR stimulation.

J Immunol (2019) 203 (4): 946–955.

  • CD69 is not required for the establishment of CD8+ TRM in every nonlymphoid tissue.

  • In the kidney, CD69 is required for CD8+ TRM regardless of immunization approach.

  • CD69 deficiency prevents generation of KLF2low TRM in the kidney.

J Immunol (2019) 203 (4): 956–963.

  • Adiponectin KO mice show increased pathology in a mouse model of IA.

  • KO mice show increased inflammatory and decreased anti-inflammatory phenotypes.

  • Increased lung inflammation in KO mice is independent of invasive fungal growth.

J Immunol (2019) 203 (4): 964–971.

  • Deficiency of NK cells leads to enhanced susceptibility to T. congolense infection.

  • NK cells mediate protection during T. congolense infection via perforin.

J Immunol (2019) 203 (4): 972–980.

  • We describe a naive-like M. tuberculosis–specific CD4+ IFN-γ+ memory T cell (TNLM).

  • TNLM provide protection equal to known memory subsets against M. tuberculosis lung infection.


J Immunol (2019) 203 (4): 981–989.

  • KLF12 deficiency does not affect NK cell development and effector functions.

  • KLF12-deficient NK cells have increased expression of Btg3 and the IL-21 receptor.

  • IL-21 induced Btg3 and inhibited KLF12-deficient NK cell proliferation.

J Immunol (2019) 203 (4): 990–1000.

  • NAFLD microenvironments increase Tim-4 expression in macrophages.

  • Tim-4 in macrophages suppresses NLRP3 inflammasome depending on PS binding motif.

  • Tim-4 promotes phosphorylation of AMPKα by interacting with LKB1.

J Immunol (2019) 203 (4): 1001–1011.

  • NAC1 enhances the virus-induced IFN signaling and activation of TBK1 and IRF3.

  • NAC1 inhibits the replication of RNA viruses.

  • NAC1 promotes the recruitment of TBK1 to MAVS upon viral infection.

J Immunol (2019) 203 (4): 1012–1020.

  • FBXO6 can negatively regulate the activation of IFN-I signaling.

  • FBXO6 interacts with and mediates IRF3 degradation independent of SCF complex.

J Immunol (2019) 203 (4): 1021–1030.

  • AZM’s immunomodulatory mechanism involves both NF-κB and STAT1 pathways.

  • AZM’s impact on STAT1 phosphorylation works in part through IKKβ.

J Immunol (2019) 203 (4): 1031–1043.

  • V-ATPase is required for ERK-mediated 15-LOX-1 expression during M2 polarization.

  • Inhibition of V-ATPase prevents 15-LOX-1–mediated SPM biosynthesis in M2 macrophages.

  • Targeting V-ATPase delays resolution in murine peritonitis with decreased SPM levels.


J Immunol (2019) 203 (4): 1044–1054.

  • Early T-BET expression is important for early acquisition of CD8+ T cell lineage–specific function.

  • T-BET expression shuts down inappropriate T cell lineage functions in activated CD8+ T cells.

  • Early T-BET expression is required for activation of specific IFN-γ transcriptional enhancers.

J Immunol (2019) 203 (4): 1055–1063.

  • The interactomes of CD2 and CD28 were identified.

  • CSK is a specific and direct interactor of activated CD28.

  • CSK regulates signaling downstream of CD28.


J Immunol (2019) 203 (4): 1064–1075.

  • Neutrophil proteomes are mapped during homeostasis or following lethal PR8 infection.

  • ISGs are first elevated in BM and then BAL neutrophils following lethal PR8 infection.

  • BAL neutrophil proteomes exhibit a modest capacity for pathogen tuning.


J Immunol (2019) 203 (4): 1076–1087.

  • LILRB1 inhibits BiTE molecule–induced cytolytic activity of human CD8+ T cells.

  • LILRB1 and PD1 express on distinct human CD8+ T cell subsets in tumors.

  • LILRB1 and PD1 blockades have synergistic effects to enhance CD8+ T cell activity.

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