PILLARS OF IMMUNOLOGY
This Pillars of Immunology article is a commentary on “Hematopoietic stem cell transplantation for severe combined immunodeficiency in the neonatal period leads to superior thymic output and improved survival,” a pivotal article written by L. A. Myers, D. D. Patel, J. M. Puck, and R. H. Buckley, and published in Blood, in 2002. https://pubmed.ncbi.nlm.nih.gov/11806989/.
IL-10 Negatively Controls the Primary T Cell Response of Tilapia by Triggering the JAK1/STAT3/SOCS3 Axis That Suppresses NF-κB and MAPK/ERK Signaling
IL-10 suppresses T cell activation, proliferation, and effector function of tilapia.
Tilapia IL-10 triggers the JAK1/STAT3/SOCS3 axis to inhibit the NF-κB and MAPK/ERK pathway.
Tilapia evolved sophisticated mechanisms to negatively regulate T cell immunity.
CgDM9CP-5-Integrin-MAPK Pathway Regulates the Production of CgIL-17s and Cgdefensins in the Pacific Oyster, Crassostrea gigas
CgDM9CP-5 was expressed at the highest level in the gill tissue of oysters.
CgDM9CP-5 exhibited binding activities to microbes as well as various PAMPs.
The CgDM9CP-5-integrin-MAPK pathway regulated the release of CgIL-17s and Cgdefensins.
IMMUNOTHERAPY AND VACCINES
Lung Resident Memory T Cells Activated by Oral Vaccination Afford Comprehensive Protection against Pneumonic Yersinia pestis Infection
Mice orally vaccinated with Yptb1(pYA5199) accumulated lung CD4 and CD8 TRM cells.
Lung TRM cells expressed IFN-γ, and IL-17A played a vital role against pneumonic plague.
Oral Yptb1(pYA5199) vaccination developed long-lived immunity in the lung.
INFECTIOUS DISEASE AND HOST RESPONSE
Identification of Cell Types and Transcriptome Landscapes of Porcine Epidemic Diarrhea Virus–Infected Porcine Small Intestine Using Single-Cell RNA Sequencing
scRNA-seq was first used to reveal transcriptome changes in PEDV-infected jejunum.
PEDV effectively infects goblet cells and decreases the expression of MUC2.
IL-33 and STAT3 play roles in PEDV inducing REG3G, which inhibits PEDV replication.
The Foot-and-Mouth Disease Virus Lb Protease Cleaves Intracellular Transcription Factors STAT1 and STAT2 to Antagonize IFN-β–Induced Signaling
FMDV leader protease inhibits IFN-β–induced innate immune response.
FMDV Lpro interacts with STAT1/2 to cleave STAT1/2 through protease activity.
252–502 aa of STAT1 and 140–150 aa of STAT2 are critical for Lpro cleavage.
Helminth Infection–Induced Increase in Virtual Memory CD8 T Cells Is Transient, Driven by IL-15, and Absent in Aged Mice
Helminth infection–driven increases in TVM cells are caused by IL-15.
The impact on TVM cells after helminth infection is not maintained into old age.
Intrinsic and extrinsic age-associated changes prevented an increase in TVM cells.
INNATE IMMUNITY AND INFLAMMATION
Extracellular CIRP Induces Novel Nectin-2+ (CD112+) Neutrophils to Promote Th1 Differentiation in Sepsis
eCIRP induces CD112 (Nectin-2)-expressing neutrophils in sepsis via the TLR4 pathway.
CD112+ neutrophils induce the Th1 phenotype when cocultured with CD4 T cells.
Lipopolysaccharide Primes Human Macrophages for Noncanonical Inflammasome-Induced Extracellular Vesicle Secretion
Noncanonical inflammasome activation triggers release of extracellular vesicles.
This EV secretion is caspase-4–, NLRP3- and type I IFN–dependent.
PGJ2 and parthenolide inhibit inflammation and EV release upon LPS transfection.
Theilovirus 3C Protease Cleaves the C-Terminal Domain of the Innate Immune RNA Sensor, Melanoma Differentiation–Associated Gene 5, and Impairs Double-Stranded RNA–Mediated IFN Response
Theilovirus 3C protease cleaves the innate immune viral sensor MDA5.
The proteolytic cleavage abrogates viral RNA recognition by MDA5.
The cleavage-resistant MDA5 gains an IFN response against Saffold virus infection.
Low-Dose Lipopolysaccharide Protects from Lethal Paramyxovirus Infection in a Macrophage- and TLR4-Dependent Process
Low-dose LPS before, but not after, respiratory viral infection increases survival.
LPS-mediated survival depends on macrophages, but not neutrophils.
LPS provides a survival advantage through type I IFN and TLR4-MyD88 signaling.
On the cover: Histograms depicting CTV dilutions of CD8 T cells from uninfected (shaded) and H. polygyrus infected (unshaded) mice after 65 h of anti-CD3/8/11a stimulation. Blue, naive T cells; yellow, virtual memory T cells; red, conventional memory T cells. Data are representative of two experiments with n = 4−5 mice per group. Hussain, T., A. Nguyen, C. Daunt, D. Thiele, E. S. Pang, J. Li, A. Zaini, M. O’Keeffe, C. Zaph, N. L. Harris, K. M. Quinn, and N. L. La Gruta. 2023. Helminth infection−induced increase in virtual memory CD8 T cells is transient, driven by IL-15, and absent in aged mice. J. Immunol. 210: 297–309.
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