IN THIS ISSUE
PILLARS OF IMMUNOLOGY
Cutting Edge: Targeting Thrombocytes to Rewire Anticancer Immunity in the Tumor Microenvironment and Potentiate Efficacy of PD-1 Blockade
Platelets alter frequency, phenotype, and function of tumor-infiltrating lymphocytes.
Inhibition of platelet activation improves CD8+ T cell–dependent tumor control.
Pretreatment with antiplatelet therapy enhances responsiveness to PD-1 blockade.
ALLERGY AND OTHER HYPERSENSITIVITIES
The Il9 CNS-25 is required for IL-9 production in mast cells and basophils.
There is differential control of the Il9 gene between mast cells and T cells.
Intestinal mast cell expansion requires Il9 CNS-25–dependent IL-9.
SP-A aids in the resolution of allergic airway inflammation.
SP-A promotes eosinophil clearance through chemotaxis and apoptosis.
Genetic variation alters the ability of SP-A to induce eosinophil apoptosis.
ANTIGEN RECOGNITION AND RESPONSES
MD-2 Homologue Recognizes the White Spot Syndrome Virus Lipid Component and Induces Antiviral Molecule Expression in Shrimp
Shrimp MD-2 homologue ML1 recognizes a lipid component of white spot syndrome virus.
Shrimp ML1 activates NF-κB signaling.
ML1 induces the expression of Vago, which is a functional analogue of IFN.
IL-11 Induces Encephalitogenic Th17 Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis
IL-11+CD4+ cells accumulate in the CSF and active brain RRMS lesions.
IL-11 increased the numbers of CNS-infiltrating IL-17+CD4+ cells in RREAE.
Passive transfer of IL-11–induced encephalitogenic CD4+ T cells induced severe RREAE.
CLINICAL AND HUMAN IMMUNOLOGY
Bidirectional Cross-Talk between Biliary Epithelium and Th17 Cells Promotes Local Th17 Expansion and Bile Duct Proliferation in Biliary Liver Diseases
Biliary epithelial cells secrete Th17-polarizing cytokines.
Biliary epithelial cells chemoattract AhR+CCR6+CD4 T cells.
Th17 cells promote local Th17 expansion and bile duct proliferation.
Early T Cell Differentiation with Well-Maintained Function across the Adult Life Course in Sub-Saharan Africa
Only 14% of CD4 or CD8 T cells of young adult Malawians were naive (CCR7+CD45RA+).
There is little age-associated accumulation of differentiated or senescent T cells.
There are robust T cell responses to viral Ags and mitogens from early 20s to late 60s.
Ancestral T Cells in Fish Require mTORC1-Coupled Immune Signals and Metabolic Programming for Proper Activation and Function
mTORC1 regulates teleost T cell activation, proliferation, and effector function.
mTORC1 links immune signals to metabolic programs in teleost T cells.
Primordial T cells in teleost have evolved sophisticated regulatory strategies
Control of Tissue-Resident Invariant NKT Cells by Vitamin A Metabolites and P2X7-Mediated Cell Death
Vitamin A negatively regulates iNKT cell population.
P2X7 upregulation by retinoic acid makes iNKT cells sensitive to cell death.
Tissue-resident iNKT cells are preferentially controlled by P2X7 activation.
Lipopolysaccharide Downregulates 11β-Hydroxysteroid Dehydrogenase 2 Expression through Inhibiting Peroxisome Proliferator–Activated Receptor-γ in Placental Trophoblasts
LPS downregulates 11β-HSD2 through inhibiting PPARγ in placental trophoblasts.
LPS promotes interaction between NF-κB p65 and PPARγ in the cytoplasm and nucleus.
Pretreatment with PPARγ agonist RSG partially alleviates LPS-induced fetal IUGR.
Efficient CD4Cre-Mediated Conditional KRas Expression in Alveolar Macrophages and Alveolar Epithelial Cells Causes Fatal Hyperproliferative Pneumonitis
CD4Cre efficiently recombines in alveolar macrophages and lung epithelial cells.
Constitutively active KRas causes T cell hyperactivation and autoimmune diseases.
CD4Cre-mediated KRas expression causes fatal hyperproliferative pneumonitis.
Mycobacterium tuberculosis PPE2 Protein Interacts with p67phox and Inhibits Reactive Oxygen Species Production
PPE2 protein of M. tuberculosis inhibits ROS production.
PPE2 protein interact with p67phox, inhibiting NADPH oxidase complex formation.
W236 in PPE2–SH3 domain is crucial for PPE2–p67phox interaction and ROS inhibition.
PLZF-deficient mice have reduced numbers of basophil progenitors and mature basophils.
PLZF-deficient basophils respond poorly to the protein allergen papain.
PLZF-deficient basophils are refractory to activation and produce less IL-4.
IMMUNE SYSTEM DEVELOPMENT
Our study shows that IL-21 plays a pleiotropic role in thymic T cell development.
IL-21 is involved in the differentiation of DN subsets as early as the DN1 stage.
Furthermore, IL-21 seems to be implicated in the emigration of SP CD4 CD8 T cells.
Clustered Mutations at the Murine and Human IgH Locus Exhibit Significant Linkage Consistent with Templated Mutagenesis
Somatic mutations in close proximity exhibit high linkage disequilibrium.
Pairs of somatic mutations within 8 bp are templated from IgHV gene segments.
Pairs of somatic mutations in non-Ig genes at the IgH locus are similarly templated.
Ig-TCRδ rearrangement expression is equivalent to canonical TCRδ in the nurse shark.
Novel lineage of TCR-associated Ig-like V segments is found in shark TCRδ locus.
Ig-TCRδ receptors are produced by intralocus and interlocus VDJ events and pair with TCRγ.
INFECTIOUS DISEASE AND HOST RESPONSE
Primary EBV infection drives highly cytotoxic virus-specific CD4+ T cell responses.
EBV-specific memory CD4+ T cells are polyfunctional but lack cytotoxic activity.
Acute EBV-specific CD4-CTLs differ transcriptionally from classical memory CD4-CTLs.
Viral infection downregulates GNAQ expression.
GNAQ deficiency increases host antiviral immunity both in vitro and in vivo.
GNAQ negatively regulates IFN-I production in a calcineurin-dependent manner.
Memory reactivation to priming Ags induces real-time immune resetting in sepsis.
Sepsis response shifts from pathogen-driven to one driven by memory reactivation.
Resetting in sepsis increases survival by a new hypoinflammatory T cell response.
Prostaglandin E2–Induced Immune Exhaustion and Enhancement of Antiviral Effects by Anti–PD-L1 Antibody Combined with COX-2 Inhibitor in Bovine Leukemia Virus Infection
PGE2 induces immune exhaustion and promotes disease progression of BLV infection.
Dual blockade of PGE2 and PD-L1 invigorates antiviral immune response in cattle.
INNATE IMMUNITY AND INFLAMMATION
Myeloid-Derived Suppressor Cells Confer Infectious Tolerance to Dampen Virus-Induced Tissue Immunoinflammation
MDSCs were identified as CD11b+Gr1lo-int in HSV1-infected mice.
In vitro–generated MDSCs controlled the severity of HSK lesions.
MDSCs promoted endogenous Treg response that also included a de novo conversion.
Phosphatase PPM1L Prevents Excessive Inflammatory Responses and Cardiac Dysfunction after Myocardial Infarction by Inhibiting IKKβ Activation
PPM1L prevents excessive inflammation and cardiac dysfunction after MI.
PPM1L binds IKKβ, inhibits its phosphorylation, and impairs NF-κB activation.
IFNs induce RIPK3-dependent cell death in the absence of RIPK1.
The IFN-stimulated gene product ZBP1 drives cell death in Ripk1−/− cells.
ZBP1 and IFN signaling contribute to perinatal lethality of Ripk1−/− mice.
The mice with constitutively activated MDA5 exhibit SMS-like bone abnormalities.
Bone resorption and bone formation are attenuated in MDA5 G821S mutant mice.
The pathogenesis is dependent on type I IFN induced by MDA5/MAVS signaling.
Tongue sole GSDME is cleaved mainly by CASP1 and induces pyroptosis.
CASP3/7 also cleave tongue sole GSDME and switch apoptosis to secondary pyroptosis.
CASP1-dependent cleavage of GSDME is preserved in a large number of teleost species.
MOLECULAR AND STRUCTURAL IMMUNOLOGY
Integrin α5β1 binds to monomeric CD40L through the trimeric interface of CD40L.
CD40L mutants defective in integrin binding act as antagonists.
Functional defects in HIGM1 mutations may be due to defective integrin binding.
Postoperative Portal Hypertension Enhances Alloimmune Responses after Living-Donor Liver Transplantation in Patients and in a Mouse Model
Postoperative portal hypertension enhances alloimmune responses after LDLT.
Immune-suppression capacity of LSECs is impaired by portal hypertension.
On the cover: Tissue segmentation (red, bile ductules; green, portal), nuclear boundaries (dark green), and cell phenotypes (circles: CD4+AhR+, blue; CD4+AhR−, red; CD4−AhR+, green; CD4−AhR−, yellow) determined by InForm algorithmic analysis of immunohistochemistry performed on an explanted liver tissue section from a primary sclerosing cholangitis liver. Jeffery, H. C., S. Hunter, E. H. Humphreys, R. Bhogal, R. E. Wawman, J. Birtwistle, M. Atif, C. J. Bagnal, G. Rodriguez Blanco, N. Richardson, S. Warner, W. B. Dunn, S. C. Afford, D. H. Adams, and Y. H. Oo. 2019. Bidirectional cross-talk between biliary epithelium and Th17 cells promotes local Th17 expansion and bile duct proliferation in biliary liver diseases. J. Immunol. 203: 1151–1159.
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