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Issues

IN THIS ISSUE

J Immunol (2019) 202 (8): 2175–2176.

BRIEF REVIEWS

J Immunol (2019) 202 (8): 2177–2187.

CUTTING EDGE

J Immunol (2019) 202 (8): 2189–2194.

CLINICAL AND HUMAN IMMUNOLOGY

J Immunol (2019) 202 (8): 2195–2209.
J Immunol (2019) 202 (8): 2210–2219.
J Immunol (2019) 202 (8): 2220–2228.

  • The Ab repertoire is diversified through the acquisition of N-glycosylation sites.

  • Frequencies of V region N-glycosylation sites are isotype and subclass dependent.

  • Elevated Fab glycosylation is an additional hallmark of TH2-like IgG4/IgE responses.

IMMUNE REGULATION

J Immunol (2019) 202 (8): 2229–2239.
J Immunol (2019) 202 (8): 2240–2253.
J Immunol (2019) 202 (8): 2254–2265.

  • IRF3 is phosphorylated by Abl kinase family.

  • c-Abl and Arg regulate innate immunity by promoting type I IFN production.

  • AIM2 inflammasome activation during Ft LVS infection is prompted by Abl kinase.

J Immunol (2019) 202 (8): 2266–2275.

IMMUNE SYSTEM DEVELOPMENT

J Immunol (2019) 202 (8): 2276–2286.

  • Shp1-deficient iNKT cells are biased toward the iNKT2/17 subsets.

  • Shp1 deficiency does not alter TCR or Slam signaling.

  • Shp1 dampens iNKT cell proliferation in response to cytokines.

J Immunol (2019) 202 (8): 2287–2295.

  • NKAP Y352 is required for association with HDAC3.

  • The interaction between NKAP and HDAC3 is critical for its function in HSCs.

  • The interaction between NKAP and HDAC3 is unimportant in some cell types.

J Immunol (2019) 202 (8): 2296–2306.

  • Sostdc1 influences tNK to mNK cell differentiation and the Ly49 receptor repertoire.

  • NK cells in Sostdc1−/− mice display impaired ability to kill β2m−/− target cells.

  • Sostdc1 expression in stromal and hematopoietic cells regulates NK cells.

IMMUNOTHERAPY AND VACCINES

J Immunol (2019) 202 (8): 2307–2319.

  • We engineered the Fc of human IgG to increase its affinity for TRIM21 by 100-fold.

  • The engineered Fc enhances cross-presentation in monocyte-derived dendritic cells.

  • Our finding may be applied to vaccine design to boost CD8 T cell–based immunity.

J Immunol (2019) 202 (8): 2320–2331.

INFECTIOUS DISEASE AND HOST RESPONSE

J Immunol (2019) 202 (8): 2332–2347.
J Immunol (2019) 202 (8): 2348–2359.

  • IFN-β promotes host resistance to M. tuberculosis via induction of NO production.

  • Capacity to inhibit IFN-β signaling correlates with mycobacterial virulence.

  • M. tuberculosis limits activation of receptor-associated tyrosine kinases TYK2 and JAK1.

INNATE IMMUNITY AND INFLAMMATION

J Immunol (2019) 202 (8): 2360–2371.
J Immunol (2019) 202 (8): 2372–2383.
J Immunol (2019) 202 (8): 2384–2396.
J Immunol (2019) 202 (8): 2397–2406.

  • Knockout of USP20 inhibits HSV-1– but not Sendai virus–triggered signaling.

  • USP20-deficient mice exhibit increased susceptibility to HSV-1 infection.

  • USP20 deconjugates K48-linked polyubiquitin chains from and thereby stabilizes MITA.

J Immunol (2019) 202 (8): 2407–2420.

  • FTRCA1 is a crucian carp–specific member of finTRIM.

  • FTRCA1 downregulates fish IFN response through lysosomal degradation of TBK1.

  • The E3 ligase activity is likely required for FTRCA1 function on TBK1 degradation.

J Immunol (2019) 202 (8): 2421–2430.
J Immunol (2019) 202 (8): 2431–2450.
J Immunol (2019) 202 (8): 2451–2459.

  • Loss of adipocyte and macrophage H2Ab1 leads to no change in metabolic phenotype.

  • Specific loss of macrophage H2Ab1 leads to improvements in glucose tolerance.

  • Adipocytes on HFD express LysM and are targeted by the LysMCre model.

MOLECULAR AND STRUCTURAL IMMUNOLOGY

J Immunol (2019) 202 (8): 2460–2472.

  • Notch favors RUNX1 and MYB recruitment to activate enhancer-dependent transcription.

  • These results decipher the mechanism for Tcrd and Tcrg silencing during β-selection.

MUCOSAL IMMUNOLOGY

J Immunol (2019) 202 (8): 2473–2481.
J Immunol (2019) 202 (8): 2482–2492.

TRANSPLANTATION

J Immunol (2019) 202 (8): 2493–2501.

NOVEL IMMUNOLOGICAL METHODS

J Immunol (2019) 202 (8): 2502–2510.

CORRECTIONS

J Immunol (2019) 202 (8): 2511.
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