CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.

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Splenic CD169+ macrophages trap and prevent early Lm replication and spread. Splenic CD169+ macrophages trap and prevent early Lm replication and spread.

FIP200 loss links to poor autophagy and high apoptosis in naïve T cells in tumor. FIP200 loss links to poor autophagy and high apoptosis in naïve T cells.

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FIP200 maintains microRNA1198-5p expression via Ago2 in naïve T cells.

NFATc2-deficient mice do not eliminate skin C. albicans infections.

Specific depletion of CD4-DTR–derived CD4 T cells.

Splenic CD169+ macrophages express a unique gene profile.

The TGF-β pathway is activated in the skin after C

CCR2+ monocytes are a relevant source of type I IFN in response to Af.

FIP200 controls Bak expression via maintaining microRNA1198-5p expression. FIP200 controls Bak expression via maintaining microRNA1198-5p expression. (A)

Regulatory CD4+ T cell–derived IL-10 is important for B cell differentiation and the GC response. Regulatory CD4+ T cell–derived IL-10 is important for.

CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.

LV activation of DCs and subsequent CD8+ T cell priming are dependent on STING and cGAS but not on MyD88, TRIF, or MAVS. LV activation of DCs and subsequent.

Altered distribution of γδT IELs in GPR55-deficient mice.

FIP200 loss links to poor autophagy and high apoptosis in naïve T cells in tumor. FIP200 loss links to poor autophagy and high apoptosis in naïve T cells.

Human PBMC-derived MERS-CoV–specific T cells are multifunctional.

Cytosolic entry of Lm required for CD8α+ DC recruitment.

Virus-specific T cell responses are detected in all MERS survivors.

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Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.

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PD-L1 selectively marks circulating NCMs.

PD-L1 expression is maintained on NCMs under inflammatory conditions and PD-L1+NCMs are found in TLOs. PD-L1 expression is maintained on NCMs under inflammatory.

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Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. (A)

CD169+ macrophages mediate the transport of bacteria to T cell zones by trans-infecting CD8α+ DCs. CD169+ macrophages mediate the transport of bacteria.

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RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development. RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development.

RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.

CD25 expression identifies two transcriptionally distinct subsets of very early effector cells. CD25 expression identifies two transcriptionally distinct.

CypD-deficient mice are susceptible to Mtb infection.

CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.

Fig. 3 FcRL1 is passively recruited into B cell immunological synapses upon BCR engagement in primary spleen B cells. FcRL1 is passively recruited into.

Fig. 6 SNP rs is a functional SNP in 22Rv1 cells.

Tfr cells respond better to immunization with self-antigens than with foreign antigens. Tfr cells respond better to immunization with self-antigens than.

TRPML1 is required for fast DC migration, chemotaxis, and arrival at the LNs. TRPML1 is required for fast DC migration, chemotaxis, and arrival at the.

Human Tfr cells do not express CD25.

CD25 expression predicts effector and memory differentiation.

Fig. 2 IRF8 is expressed in CD68+ macrophages after SCI.

Fig. 1 Deficient CD73 and CD39 expressions and extracellular adenosine concentration in BM of OVX animals. Deficient CD73 and CD39 expressions and extracellular.

Fig. 5. Vascularization of human liver seed grafts.

Chronic Treg reduction results in dermal fibrosis.

miR-146a is highly expressed selectively on γδ27− T cells.

Impact of FRC-specific Myd88 ablation on omental FALC organization.

Fig. 1. Paclitaxel delays tumor growth and promotes infiltration of TIE2hi/VEGFhi macrophages and TMEM assembly. Paclitaxel delays tumor growth and promotes.

Fibroblast activation in WT and NFATc2-deficient mice.

Expansion of omental FRCs and FALC remodeling after intraperitoneal exposure to bacterial antigen. Expansion of omental FRCs and FALC remodeling after.

Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice. Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice.

REV-ERBα deficiency reduces frequency and number of NKp46+ ILC3s.

Ectopic Lin28b functionally replaces CD19 in B cell development and maintenance. Ectopic Lin28b functionally replaces CD19 in B cell development and maintenance.

Meningeal γδ T cells are biased toward IL-17 production.

Fetal-derived γδ T cells infiltrate the meninges from birth.

CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis. CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis.

Fig. 1 TH17 cell differentiation was severely impaired in Cxxc1-deficient mice. TH17 cell differentiation was severely impaired in Cxxc1-deficient mice.

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CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. (A and B) Splenic Lm quantification of WT, Batf3−/−, CD169-DTR, or CD169-DTR–Batf3−/− mice at (A) 12 hpi and (B) 24 hpi. Each symbol represents individual mouse. Data are shown as means ± SEM (*P < 0.05, Mann-Whitney test). (C) Confocal images of spleen sections from WT, Batf3−/−, CD169-DTR, or CD169-DTR–Batf3−/− mice at 24 hpi. Spleen sections stained for Lm (red), F4/80 (blue), and CD8 (yellow). Lm are rendered with spots. Scale bars, 100 μm. (D) Frequency of Lm found in splenic T cell zones at 24 hpi in WT, CD169-DTR, or CD169-DTR–Batf3−/− mice. Data are shown as means ± SEM. (E) Lm quantification in the spleens of WT, Batf3−/−, CD169-DTR, or CD169-DTR–Batf3−/− mice at 1 hpi. Each symbol represents an individual mouse. Data are shown as means ± SEM (**P < 0.005, Mann-Whitney test). (F) Frequency of intracellular Lm located within CD169+ macrophages in WT or Batf3−/− mice at 3 hpi. All data are representative of two to four separate experiments. Oriana A. Perez et al. Sci. Immunol. 2017;2:eaah5520 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works