scholarly journals Generation of Mice Deficient for Macrophage Galactose- and N-Acetylgalactosamine-Specific Lectin: Limited Role in Lymphoid and Erythroid Homeostasis and Evidence for Multiple Lectins

2002 ◽  
Vol 22 (14) ◽  
pp. 5173-5181 ◽  
Author(s):  
Thandi M. Onami ◽  
Meei-Yun Lin ◽  
Dawne M. Page ◽  
Shirley A. Reynolds ◽  
Carol D. Katayama ◽  
...  
Keyword(s):  
Immune Responses ◽  
Cd8 T Cells ◽  
Blood Cells ◽  
Mouse Macrophage ◽  
Adaptive Immune Responses ◽  
Targeted Disruption ◽  
Thymic Development ◽  
Adaptive Immune ◽  
Macrophage Receptors ◽  
Deficient Mice

ABSTRACT Macrophage receptors function in pattern recognition for the induction of innate immunity, in cellular communication to mediate the regulation of adaptive immune responses, and in the clearance of some glycosylated cells or glycoproteins from the circulation. They also function in homeostasis by initiating the engulfment of apoptotic cells. Evidence has suggested that macrophage receptors function to recognize cells that are destined for programmed cell death but not yet overtly apoptotic. We have examined the function of a macrophage receptor specific for unsialylated glycoproteins, known as the mouse macrophage galactose- and N-acetylgalactosamine-specific lectin (mMGL) (Ii et al., J. Biol. Chem. 265:11295-11298, 1990; Sato et al., J. Biochem. [Tokyo] 111:331-336, 1992; Yamamoto et al., Biochemistry 33:8159-8166, 1994). With targeted disruption, we tested whether mMGL is necessary for macrophage function, controlled thymic development, the loss of activated CD8 T cells, and the turnover of red blood cells. Evidence indicates that mMGL may play a nonessential role in several of these macrophage functions. Experiments are presented that indicate the existence of another galactose- and N-acetylgalactosamine-recognizing lectin distinct from mMGL. This may explain the absence of a strong phenotype in mMGL-deficient mice.

scholarly journals Metal-induced delayed type hypersensitivity responses potentiate particle induced osteolysis in a sex and age dependent manner

PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0251885
Author(s):  
Lauryn Samelko ◽  
Marco Caicedo ◽  
Kyron McAllister ◽  
Joshua Jacobs ◽  
Nadim James Hallab
Keyword(s):  
Immune Responses ◽  
Nlrp3 Inflammasome ◽  
Inflammatory Responses ◽  
Delayed Type Hypersensitivity ◽  
Adaptive Immune Responses ◽  
Male And Female ◽  
Female Mice ◽  
Adaptive Immune ◽  
Caspase 1 ◽  
Deficient Mice

It is widely recognized that innate macrophage immune reactions to implant debris are central to the inflammatory responses that drive biologic implant failure over the long term. Less common, adaptive lymphocyte immune reactions to implant debris, such as delayed type hypersensitivity (DTH), can also affect implant performance. It is unknown which key patient factors, if any, mediate these adaptive immune responses that potentiate particle/macrophage mediated osteolysis. The objective of this investigation was to determine to what degree known adaptive immune responses to metal implant debris can affect particle-induced osteolysis (PIO); and if this pathomechanism is dependent on: 1) innate immune danger signaling, i.e., NLRP3 inflammasome activity, 2) sex, and/or 3) age. We used an established murine calvaria model of PIO using male and female wild-type C57BL/6 vs. Caspase-1 deficient mice as well as young (12–16 weeks old) vs. aged (18–24 months old) female and male C57BL/6 mice. After induction of metal-DTH, and Cobalt-alloy particle (ASTM F-75, 0.4um median diameter) calvaria challenge, bone resorption was assessed using quantitative micro-computed tomography (micro-CT) analysis and immune responses were assessed by measuring paw inflammation, lymphocyte transformation test (LTT) reactivity and adaptive immune cytokines IFN-gamma and IL-17 (ELISA). Younger aged C57BL/6 female mice exhibited the highest rate and severity of metal sensitivity lymphocyte responses that also translated into higher PIO compared to any other experimental group. The absence of inflammasome/caspase-1 activity significantly suppressed DTH metal-reactivity and osteolysis in both male and female Caspase-1 deficient mice. These murine model results indicate that young female mice are more predisposed to metal-DTH augmented inflammatory responses to wear debris, which is highly influenced by active NLRP3 inflammasome/caspase-1 danger signaling. If these results are clinically meaningful for orthopedic patients, then younger female individuals should be appropriately assessed and followed for DTH derived peri-implant complications.

scholarly journals 62: Sensing and Alarm Function of Mucosal Memory CD8 T Cells Trigger Innate and Adaptive Immune Responses

2015 ◽  
Vol 143 (suppl_1) ◽  
pp. A034-A034 ◽  
Author(s):  
Jason M. Schenkel ◽  
Kathryn A. Fraser ◽  
Lalit K. Beura ◽  
Kristen E. Pauken ◽  
David Masopust ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Cd8 T Cells ◽  
Adaptive Immune Responses ◽  
Memory Cd8 T Cells ◽  
Adaptive Immune

scholarly journals Comparative ability of IL-12 and IL-28B to regulate Treg populations and enhance adaptive cellular immunity

Blood ◽  
2009 ◽  
Vol 113 (23) ◽  
pp. 5868-5877 ◽  
Author(s):  
Matthew P. Morrow ◽  
Panyupa Pankhong ◽  
Dominick J. Laddy ◽  
Kimberly A. Schoenly ◽  
Jian Yan ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Cd8 T Cells ◽  
Dna Vaccination ◽  
Vaccine Adjuvant ◽  
Cell Populations ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Strong Candidate ◽  
First Time

Abstract Improving the potency of immune responses is paramount among issues concerning vaccines against deadly pathogens. IL-28B belongs to the newly described interferon lambda (IFNλ) family of cytokines, and has not yet been assessed for its potential ability to influence adaptive immune responses or act as a vaccine adjuvant. We compared the ability of plasmid-encoded IL-28B to boost immune responses to a multiclade consensus HIV Gag plasmid during DNA vaccination with that of IL-12. We show here that IL-28B, like IL-12, is capable of robustly enhancing adaptive immunity. Moreover, we describe for the first time how IL-28B reduces regulatory T-cell populations during DNA vaccination, whereas IL-12 increases this cellular subset. We also show that IL-28B, unlike IL-12, is able to increase the percentage of splenic CD8+ T cells in vaccinated animals, and that these cells are more granular and have higher antigen-specific cytolytic degranulation compared with cells taken from animals that received IL-12 as an adjuvant. Lastly, we report that IL-28B can induce 100% protection from mortality after a lethal influenza challenge. These data suggest that IL-28B is a strong candidate for further studies of vaccine or immunotherapy protocols.

scholarly journals Undaria pinnatifida Fucoidan-Rich Extract Induces Both Innate and Adaptive Immune Responses

2019 ◽  
Vol 14 (8) ◽  
pp. 1934578X1987372
Author(s):  
Hwan H. Lee ◽  
Yoo J. Cho ◽  
Daeung Yu ◽  
Donghwa Chung ◽  
Gun-Hee Kim ◽  
...  
Keyword(s):  
Immune Responses ◽  
Cd8 T Cells ◽  
Undaria Pinnatifida ◽  
Plasma Concentrations ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Tnf Α ◽  
Ifn Γ

Fucoidans are widely used as an ingredient of dietary supplements. We investigated the immune stimulatory activities of Undaria pinnatifida ( Alariaceae) fucoidan-rich extract (UPF-RE) in vitro as well as in vivo . In vitro, the extract stimulated Raw 264.7 cells to produce significant nitric oxide (NO) metabolites and cytokines (TNF-α, IL-1α, IL-1β, and IL-6). It also induced the proliferation of primary mouse splenocytes and the secretion of IL-4, which correlated with the phosphorylation of Extracellular-signal-regulated kinase (ERK) protein. In in vivo experiments, first, 50 mg/kg of 3 different types of UPF-RE, DSU02, DSU02L (low molecular weight, <3 kDa), and DSU02H (high molecular weight, >10 kDa), were orally administered to C57BL/6 mice. After 14 days, the frequencies of CD3+, CD4+, and CD8+ T cells and NK cells from each group were analyzed. Plasma concentrations of TNF-α and IFN-γ were determined. The frequencies of CD3+ and CD4+ showed a statistically significant increase in splenocytes isolated from the DSU02 and DSU02H groups. Also, there was significant production of TNF-α and IFN-γ from the DSU02 group. Second, 3 different concentrations of DSU02 (50, 100, and 150 mg/kg) were orally administered. After 14 days, the proliferative capacity of CD3+, CD4+, and CD8+ T cells was investigated, and the plasma concentrations of IgM and total IgG were determined. Plasma concentration of IgM from the DSU02 150 mg/kg group was statistically significantly higher compared with that from the other groups. We suggest that UPF-RE could be a good candidate for a natural immune stimulator to induce innate as well as adaptive immune responses.

scholarly journals Disrupting Bordetella Immunosuppression Reveals a Role for Eosinophils in Coordinating the Adaptive Immune Response in the Respiratory Tract

2020 ◽  
Vol 8 (11) ◽  
pp. 1808 ◽  
Author(s):  
Monica C. Gestal ◽  
Uriel Blas-Machado ◽  
Hannah M. Johnson ◽  
Lily N. Rubin ◽  
Kalyan K. Dewan ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Respiratory Tract ◽  
Respiratory Pathogens ◽  
Adaptive Immune Responses ◽  
Eosinophil Recruitment ◽  
Adaptive Immune ◽  
Deficient Mice ◽  
Lymphoid Aggregates ◽  
Allergy And Asthma

Recent findings revealed pivotal roles for eosinophils in protection against parasitic and viral infections, as well as modulation of adaptive immune responses in the gastric mucosa. However, the known effects of eosinophils within the respiratory tract remain predominantly pathological, associated with allergy and asthma. Simulating natural respiratory infections in mice, we examined how efficient and well-adapted pathogens can block eosinophil functions that contribute to the immune response. Bordetella bronchiseptica, a natural pathogen of the mouse, uses the sigma factor btrS to regulate expression of mechanisms that interfere with eosinophil recruitment and function. When btrS is disrupted, immunomodulators are dysregulated, and eosinophils are recruited to the lungs, suggesting they may contribute to much more efficient generation of adaptive immunity induced by this mutant. Eosinophil-deficient mice failed to produce pro-inflammatory cytokines, to recruit lymphocytes, to organize lymphoid aggregates that resemble Bronchus Associated Lymphoid Tissue (BALT), to generate an effective antibody response, and to clear bacterial infection from the respiratory tract. Importantly, the failure of eosinophil-deficient mice to produce these lymphoid aggregates indicates that eosinophils can mediate the generation of an effective lymphoid response in the lungs. These data demonstrate that efficient respiratory pathogens can block eosinophil recruitment, to inhibit the generation of robust adaptive immune responses. They also suggest that some post-infection sequelae involving eosinophils, such as allergy and asthma, might be a consequence of bacterial mechanisms that manipulate their accumulation and/or function within the respiratory tract.

scholarly journals Splenic Dendritic Cells Survey Red Blood Cells for Missing Self-CD47 to Trigger Adaptive Immune Responses

Immunity ◽  
2015 ◽  
Vol 43 (4) ◽  
pp. 764-775 ◽  
Author(s):  
Tangsheng Yi ◽  
Jianhua Li ◽  
Hsin Chen ◽  
Jiaxi Wu ◽  
Jinping An ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Missing Self

scholarly journals Characterization of Innate and Adaptive Immune Responses in PYNOD-Deficient Mice

2018 ◽  
Vol 2 (4) ◽  
pp. 129-141
Author(s):  
Shinsuke Nakajima ◽  
Ryu Imamura ◽  
Miya Yoshino ◽  
Mayumi Sakurai ◽  
Kohsuke Tsuchiya ◽  
...  
Keyword(s):  
Immune Responses ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Deficient Mice

scholarly journals Yellow fever vaccine YF-17D activates multiple dendritic cell subsets via TLR2, 7, 8, and 9 to stimulate polyvalent immunity

2006 ◽  
Vol 203 (2) ◽  
pp. 413-424 ◽  
Author(s):  
Troy Querec ◽  
Soumaya Bennouna ◽  
Sefik Alkan ◽  
Yasmina Laouar ◽  
Keith Gorden ◽  
...  
Keyword(s):  
Immune Responses ◽  
Yellow Fever ◽  
Yellow Fever Vaccine ◽  
Interferon Α ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Immunological Mechanisms ◽  
History Of ◽  
History Of Use ◽  
Deficient Mice

The live attenuated yellow fever vaccine 17D (YF-17D) is one of the most effective vaccines available, with a 65-yr history of use in &gt;400 million people globally. Despite this efficacy, there is presently no information about the immunological mechanisms by which YF-17D acts. Here, we present data that suggest that YF-17D activates multiple Toll-like receptors (TLRs) on dendritic cells (DCs) to elicit a broad spectrum of innate and adaptive immune responses. Specifically, YF-17D activates multiple DC subsets via TLRs 2, 7, 8, and 9 to elicit the proinflammatory cytokines interleukin (IL)-12p40, IL-6, and interferon-α. Interestingly, the resulting adaptive immune responses are characterized by a mixed T helper cell (Th)1/Th2 cytokine profile and antigen-specific CD8+ T cells. Furthermore, distinct TLRs appear to differentially control the Th1/Th2 balance; thus, whilst MyD88-deficient mice show a profound impairment of Th1 cytokines, TLR2-deficient mice show greatly enhanced Th1 and Tc1 responses to YF-17D. Together, these data enhance our understanding of the molecular mechanism of action of YF-17D, and highlight the potential of vaccination strategies that use combinations of different TLR ligands to stimulate polyvalent immune responses.

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