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J Immunol (2021) 207 (9): 2193.

IMMUNOLOGY NOTES AND RESOURCES

J Immunol (2021) 207 (9): 2195–2202.

PILLARS OF IMMUNOLOGY

J Immunol (2021) 207 (9): 2203–2204.

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.

BRIEF REVIEWS

J Immunol (2021) 207 (9): 2205–2215.

CUTTING EDGE

J Immunol (2021) 207 (9): 2217–2222.

  • 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.

ALLERGY AND OTHER HYPERSENSITIVITIES

J Immunol (2021) 207 (9): 2223–2234.

  • 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.

AUTOIMMUNITY

J Immunol (2021) 207 (9): 2235–2244.

  • 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.

CLINICAL AND HUMAN IMMUNOLOGY

J Immunol (2021) 207 (9): 2245–2254.

  • 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.

IMMUNE REGULATION

J Immunol (2021) 207 (9): 2255–2264.

  • 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.

J Immunol (2021) 207 (9): 2265–2277.

  • 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.

J Immunol (2021) 207 (9): 2278–2287.

  • UV redistributes T cells from blood to skin-draining lymph nodes by increasing lymph node S1P.

  • Sphingosine kinase inhibitors prevent UV increases in lymph node S1P and T cells.

J Immunol (2021) 207 (9): 2288–2296.

  • IL-4 treatment induces a signalosome-independent alternate pathway for BCR signaling.

  • Lyn is autophosphorylated after IL-4 treatment in membranes.

  • PKCδ is translocated and phosphorylated by Lyn in membranes through the alternate pathway.

INNATE IMMUNITY AND INFLAMMATION

J Immunol (2021) 207 (9): 2297–2309.

  • 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-κB translocation thereby regulating iNOS and cytokine expression.

J Immunol (2021) 207 (9): 2310–2324.

  • M1 macrophages from healthy individuals and COVID-19 patients produce IFN-γ.

  • LPS stimulation of M1 macrophages significantly enhances their IFN-γ production.

  • LPS-induced IFN-γ is regulated by the PI3K-mTOR– and JNK-activated p70S6K.

J Immunol (2021) 207 (9): 2325–2336.

  • Pellino2 mediates TLR9-induced cytokine production in dendritic cells.

  • Pellino2 does not play a role in TLR9 signaling in macrophages.

  • Pellino2 is a limiting factor for TLR9 signaling in dendritic cells.

J Immunol (2021) 207 (9): 2337–2346.

  • 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.

J Immunol (2021) 207 (9): 2347–2358.

  • 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.

J Immunol (2021) 207 (9): 2359–2373.

  • 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.

J Immunol (2021) 207 (9): 2374–2384.

  • LAG3 deficiency in dendritic cells is associated with increased glycolysis.

  • LAG3 deficiency in dendritic cells enhances naive T cell priming.

CORRECTIONS

J Immunol (2021) 207 (9): 2385–2386.
J Immunol (2021) 207 (9): 2387.
J Immunol (2021) 207 (9): 2388–2389.
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