PILLARS OF IMMUNOLOGY
CLINICAL AND HUMAN IMMUNOLOGY
A senescent IPF lung microenvironment impairs differentiation and function of NK cells.
NK cells are pivotal for senescent cell clearance and the resolution of fibrosis.
Immunosequencing and Profiling of T Cells at the Maternal–Fetal Interface of Women with Preterm Labor and Chronic Chorioamnionitis
The decidual TCR repertoire is altered in women with preterm labor.
Specific T cell clonotypes are associated with chronic placental inflammation.
Choriodecidual T cells can respond to maternal and fetal Ags in vitro.
Vancomycin-altered gut microbiome enhances liver iNKT cell function.
Vancomycin treatment affects IL-18 production by CSF-1R+ macrophages.
Liver iNKT cell function is controlled by IL-18–producing CSF-1R+ macrophages.
Insulin-like Growth Factor-1 Synergizes with IL-2 to Induce Homeostatic Proliferation of Regulatory T Cells
IGF1 and IL-2 expand thymically-derived Tregs both in vitro and in vivo.
IGF1 and IL-2/7 augment naive human Treg/Tconv proliferation for gene editing.
INFECTIOUS DISEASE AND HOST RESPONSE
cGAS–STING Pathway Activation during Trypanosoma cruzi Infection Leads to Tissue-Dependent Parasite Control
Trypanosoma cruzi infection triggers a modest cGAS–STING-mediated IFN-I response.
The muted IFN-I response results from a limited triggering, not active suppression.
cGAS–STING activation by T. cruzi has both proparasite and antiparasite consequences.
INNATE IMMUNITY AND INFLAMMATION
IL-33 Orchestrated the Interaction and Immunoregulatory Functions of Alternatively Activated Macrophages and Regulatory T Cells In Vitro
IL-33 polarizes macrophages to a full AAM phenotype only in synergy with IL-4 in vitro.
Copolarized AAM-induced Treg interacted with macrophages in a feedback loop.
TGF-β is a key mediator of the immunoregulatory functions of IL-33 on AAM and Treg.
A12 (AAAAAAAAAAAA) interacts with eCIRP, preventing eCIRP’s binding to TLR4.
A12 significantly decreases eCIRP-induced sterile inflammation.
Treating septic mice with A12 ameliorates ALI and improves their survival.
Nestin+ Mesenchymal Stromal Cells Fibrotic Transition Mediated by CD169+ Macrophages in Bone Marrow Chronic Graft-versus-Host Disease
BM is a cGVHD target with abnormal hematopoiesis, fibrosis, and IgG deposition.
BM macrophages promote MSC migration and transition during cGVHD development.
On the cover: Nestin knockdown in bone marrow of murine chronic graft-versus-host disease attenuates myelofibrosis demonstrated by less collagen deposition. Zhang, H., J. Liu, Y. Sun, J. Huang, H. Qi, R. Shao, Q. Wu, Q. Jiang, R. Fu, Q. Liu, and H. Jin. 2023. Nestin+ mesenchymal stromal cells fibrotic transition mediated by CD169+ macrophages in bone marrow chronic graft-versus-host disease. J. Immunol. 211: 1154–1166.
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