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

Slides:



Advertisements
Similar presentations
Dominant IL-21 expression in TFH cells correlate with B cell pathology in HIV-infected LNs. Dominant IL-21 expression in TFH cells correlate with B cell.
Advertisements

Fibroblast activation in WT and NFATc2-deficient mice.
Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic mice. Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic.
Splenic CD169+ macrophages trap and prevent early Lm replication and spread. Splenic CD169+ macrophages trap and prevent early Lm replication and spread.
IFN-γ antagonizes TGF-β in vivo.
FIP200 deficiency alters mitochondria activation and ROS production in T cells. FIP200 deficiency alters mitochondria activation and ROS production in.
Self-folding triangular devices at two scales.
IFN-γ activates the fibrinolytic system.
Neutrophil antifungal response in CCR2-depleted mice is rescued by adoptive transfer of CCR2+ monocytes or by treatment with recombinant IFNs. Neutrophil.
CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.
CD169+ macrophages play a critical role in mediating innate immune cell reorganization. CD169+ macrophages play a critical role in mediating innate immune.
NFAT activation in innate immune cells dictates the sterilization of C
Both type I and III IFNR signaling are essential for protection against IA. Both type I and III IFNR signaling are essential for protection against IA.
Antitumor effect of local cancer immunotherapy treatment toward distant B16F10 tumors. Antitumor effect of local cancer immunotherapy treatment toward.
The TGF-β pathway is activated in the skin after C
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.
Examples of AEGIS autonomous target selection.
Mice with neutrophil-specific deletion of IFNLR1 or STAT1 succumb to IA. Mice with neutrophil-specific deletion of IFNLR1 or STAT1 succumb to IA. Conditional.
Human PBMC-derived MERS-CoV–specific T cells are multifunctional.
Cytosolic entry of Lm required for CD8α+ DC recruitment.
Platelets are required for hFcγRIIA-induced anaphylaxis.
NRP1-expressing myeloid cells influence adipocyte hypertrophy, development of fatty liver, and CLSs. NRP1-expressing myeloid cells influence adipocyte.
Reduced FOXO1 expression in GC B cells from mice lacking regulatory CD4+ T cell–derived IL-10. Reduced FOXO1 expression in GC B cells from mice lacking.
Tfr cells robustly secrete IL-10 after acute viral infection.
Tfr cell–derived IL-10 is important for B cell differentiation and the GC response. Tfr cell–derived IL-10 is important for B cell differentiation and.
Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.
NFAT activation in innate immune cells dictates the sterilization of C
BAP1 deficiency results in thymic atrophy and loss of thymocyte populations. BAP1 deficiency results in thymic atrophy and loss of thymocyte populations.
IFN-γ antagonizes TGF-β in vivo.
Evidence for platelet activation during human drug-induced anaphylaxis
NCMs regulate T cell survival in TLOs via PD-L1.
PD-L1 selectively marks circulating NCMs.
Antitumor effect of local cancer immunotherapy treatment in various tumor models. Antitumor effect of local cancer immunotherapy treatment in various tumor.
Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. (A)
Fig. 3 Intrarenal and RDLN lymphangiogenesis accompanied by lymphocyte expansion in the kidney, RDLN, and spleen. Intrarenal and RDLN lymphangiogenesis.
Fig. 3. Features of PH in KRasLA2 transgenic mice.
CD169+ macrophages mediate the transport of bacteria to T cell zones by trans-infecting CD8α+ DCs. CD169+ macrophages mediate the transport of bacteria.
Platelet-released serotonin contributes to hypothermia in mice undergoing HA-hIgG–dependent anaphylaxis. Platelet-released serotonin contributes to hypothermia.
IFN-γ activates the fibrinolytic system.
Genetic EGFR ablation in K-RAS–mutated lung AC reduces tumor growth
Vaccine MN confer protective innate and adaptive immunity.
Innate immune and fibrinolytic systems cooperate also during bacterial infections. Innate immune and fibrinolytic systems cooperate also during bacterial.
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.
Liver fibrosis after CCl4 injury in 5αR1-KO and WT mice.
Autophagy protein abundance, but not autophagy flux, is altered in Cnot3-depleted heart. Autophagy protein abundance, but not autophagy flux, is altered.
RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.
CypD-deficient mice are susceptible to Mtb infection.
Tfr cells respond better to immunization with self-antigens than with foreign antigens. Tfr cells respond better to immunization with self-antigens than.
Type I and III IFNR expression on hematopoietic cells is required for protection against IA. Type I and III IFNR expression on hematopoietic cells is required.
AEGIS autonomous targeting process.
Examples of AEGIS autonomous target selection.
Functional characterization of multidonor class antibodies.
CD25 expression predicts effector and memory differentiation.
GSDMD localizes to the plasma membrane and is processed during NET formation. GSDMD localizes to the plasma membrane and is processed during NET formation.
Neutrophil antifungal response in CCR2-depleted mice is rescued by adoptive transfer of CCR2+ monocytes or by treatment with recombinant IFNs. Neutrophil.
Fig. 4 Alternate-day ocular dosing with DECON curbs HSV-1 in a murine model of ocular infection. Alternate-day ocular dosing with DECON curbs HSV-1 in.
Fig. 2 NDR2-deficient mice are more vulnerable to RNA viral infection.
Chronic Treg reduction results in dermal fibrosis.
Fig. 2 Neonatal ZIKV infection induces seizures in young mice and increases susceptibility to chemically induced seizures in adult mice. Neonatal ZIKV.
Impact of FRC-specific Myd88 ablation on omental FALC organization.
Fibroblast activation in WT and NFATc2-deficient mice.
Fig. 3 Superiority of BAFF-R versus CD19-CAR T cells in a Burkitt lymphoma model is not due to greater tumor antigen density. Superiority of BAFF-R versus.
Fig. 3 MCA-mediated neutrophil recruitment accelerates bacterial clearance in the skin. MCA-mediated neutrophil recruitment accelerates bacterial clearance.
Meningeal γδ T cell homeostasis is independent of inflammatory signals
Fig. 6 tlr2 is necessary for SASP activation in vivo.
Fig. 2 Cxxc1 deficiency restricts T cell–mediated autoimmunity and increases sensitivity to C. rodentium infection. Cxxc1 deficiency restricts T cell–mediated.
CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis. CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis.
Cxxc1-deficient TH17 cells exhibit a Treg cell–like expression profile
Presentation transcript:

NFATc2-deficient mice do not eliminate skin C. albicans infections. NFATc2-deficient mice do not eliminate skin C. albicans infections. (A) Lesions in WT and NFATc2-deficient mice at the indicated time points after C. albicans hyphae injection in the deep derma. WT animals (top) undergo ulceration and C. albicans elimination, whereas NFATc2-deficient mice (bottom) develop a persistent abscess. (B) Kaplan-Meier curve showing the percentage of WT and NFATc2-deficient mice undergoing ulceration after C. albicans administration at the indicated time points; n = 10; log-rank test. Results are representative of at least six independent experiments. (C) Hematoxylin and eosin staining of WT (top) and NFATc2-deficient (bottom) mouse skin lesions at the indicated time points after C. albicans infections. Larger magnification of selected areas of the same section are shown to evidence granulocyte recruitment (left). PicroSirius Red staining is also shown to evidence collagen depositions (right, red deposits) and periodic acid–Schiff (PAS) staining to evidence Candida. See also fig. S2 for higher magnifications. Representative histological sections of four independent experiments are shown; see also fig. S3 (A and B). (D) WT and RAG-2–deficient mice respond similarly to primary skin infections with C. albicans. The Kaplan-Meier curve shows the percentage of WT and RAG-2–deficient mice undergoing ulceration after C. albicans administration at the indicated time points; n = 18 per group. (E) Digital image analysis quantification of collagen staining. Five fields from two sections (24 hours after infection) of two independent experiments were analyzed. The analyzed fields covered the entire sections excluding the skin. Means and SEM are depicted. n = 5; statistical significance, two-tailed t test. William Santus et al. Sci. Immunol. 2017;2:eaan2725 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works