scholarly journals Role of Macrophages in the Altered Epithelial Function during a Type 2 Immune Response Induced by Enteric Nematode Infection

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e84763 ◽  
Author(s):  
Luigi Notari ◽  
Diana C. Riera ◽  
Rex Sun ◽  
Jennifer A. Bohl ◽  
Leon P. McLean ◽  
...  
Keyword(s):  
Immune Response ◽  
Nematode Infection ◽  
Type 2 Immune Response

Type 2 immune response associated with silicosis is not instrumental in the development of the disease

2007 ◽  
Vol 292 (1) ◽  
pp. L107-L113 ◽  
Author(s):  
Pierre Misson ◽  
Frank Brombacher ◽  
Monique Delos ◽  
Dominique Lison ◽  
Francois Huaux
Keyword(s):  
Immune Response ◽  
Lung Fibrosis ◽  
Receptor Expression ◽  
Fibrotic Disease ◽  
Pulmonary Response ◽  
Type 2 Immune Response ◽  
Ifn Γ

It has been proposed that the development of lung fibrosis is associated with a T helper type 2 response, mainly characterized by IL-4 and IL-13 production. We investigated the potential role of type 2 immune polarization in the silicotic process and examined the pulmonary response to silica particles in mice genetically deficient for IL-4. We found that IL-4−/− mice were not protected against the development of silicosis, suggesting that IL-4 is not essential for the development of this fibrotic disease. By evaluating the intensity of silica-induced lung fibrosis in mice deficient for IL-4 receptor α (IL-4Rα), we showed that the establishment of pulmonary fibrosis was independent of both IL-4 and IL-13. Strong impairment of the type 2 immune response (IgG1) in the lungs of IL-4−/− and IL-4Rα−/− mice did not affect the development of the disease. Measurement of IL-13α2 receptor expression and IgG2a, IL-12p70, and IFN-γ levels in silica-treated IL-4−/− and IL-4Rα−/− animals showed that the development of silicosis was not related to an IL-13 signaling pathway or a switch to a type 1 response in deficient animals. Our data clearly indicate that the type 2 immune response associated with silicosis in mice is not required for the development of this inflammatory and fibrotic disease.

scholarly journals “The Pruritogenic Role of the Type 2 Immune Response in Diseases Associated with Chronic Itch”

2021 ◽  
Author(s):  
Giuseppe Ingrasci ◽  
Zoe M. Lipman ◽  
Ahmed A. Hawash ◽  
Giampiero Girolomoni ◽  
Gil Yosipovitch
Keyword(s):  
Immune Response ◽  
Chronic Itch ◽  
Type 2 Immune Response

Role of NKT Cells in the Regulation of Ongoing Type 2 Immune Response

2009 ◽  
pp. 151-165
Author(s):  
Christelle Faveeuw ◽  
Thomas Roumier ◽  
Monique Capron ◽  
David Dombrowicz
Keyword(s):  
Immune Response ◽  
Nkt Cells ◽  
Type 2 Immune Response

scholarly journals The Role of the IL-4 Signaling Pathway in Traumatic Nerve Injuries

2021 ◽  
pp. 154596832110010
Author(s):  
John M. Daines ◽  
Lauren Schellhardt ◽  
Matthew D. Wood
Keyword(s):  
Immune Response ◽  
Peripheral Nerve ◽  
Signaling Pathway ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Soft Tissues ◽  
Critical Element ◽  
Type 2 Immune Response

Following traumatic peripheral nerve injury, adequate restoration of function remains an elusive clinical goal. Recent research highlights the complex role that the immune system plays in both nerve injury and regeneration. Pro-regenerative processes in wounded soft tissues appear to be significantly mediated by cytokines of the type 2 immune response, notably interleukin (IL)-4. While IL-4 signaling has been firmly established as a critical element in general tissue regeneration during wound healing, it has also emerged as a critical process in nerve injury and regeneration. In this context of peripheral nerve injury, endogenous IL-4 signaling has recently been confirmed to influence more than leukocytes, but including also neurons, axons, and Schwann cells. Given the role IL-4 plays in nerve injury and regeneration, exogenous IL-4 and/or compounds targeting this signaling pathway have shown encouraging preliminary results to treat nerve injury or other neuropathy in rodent models. In particular, the exogenous stimulation of the IL-4 signaling pathway appears to promote postinjury neuron survival, axonal regeneration, remyelination, and thereby improved functional recovery. These preclinical data strongly suggest that targeting IL-4 signaling pathways is a promising translational therapy to augment treatment approaches of traumatic nerve injury. However, a better understanding of the type 2 immune response and associated signaling networks functioning within the nerve injury microenvironment is still needed to fully develop this promising therapeutic avenue.

A non-canonical type 2 immune response coordinates tuberculous granuloma formation and epithelialization

Cell ◽  
2021 ◽  
Author(s):  
Mark R. Cronan ◽  
Erika J. Hughes ◽  
W. Jared Brewer ◽  
Gopinath Viswanathan ◽  
Emily G. Hunt ◽  
...  
Keyword(s):  
Immune Response ◽  
Granuloma Formation ◽  
Type 2 Immune Response ◽  
Tuberculous Granuloma ◽  
Canonical Type

scholarly journals Dairy Heifers Naturally Exposed toFasciola hepaticaDevelop a Type 2 Immune Response and Concomitant Suppression of Leukocyte Proliferation

2017 ◽  
Vol 86 (1) ◽  
Author(s):  
John Graham-Brown ◽  
Catherine Hartley ◽  
Helen Clough ◽  
Aras Kadioglu ◽  
Matthew Baylis ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Peripheral Blood ◽  
Serum Antibody ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mixed Effect ◽  
Content Type ◽  
Grazing Season ◽  
Type 2 Immune Response

ABSTRACTFasciola hepaticais a parasitic trematode of global importance in livestock. Control strategies reliant on anthelmintics are unsustainable due to the emergence of drug resistance. Vaccines are under development, but efficacies are variable. Evidence from experimental infection suggests that vaccine efficacy may be affected by parasite-induced immunomodulation. Little is known about the immune response toF. hepaticafollowing natural exposure. Hence, we analyzed the immune responses over time in calves naturally exposed toF. hepaticainfection. Cohorts of replacement dairy heifer calves (n= 42) with no prior exposure toF. hepatica, on three commercial dairy farms, were sampled over the course of a grazing season. Exposure was determined through anF. hepatica-specific serum antibody enzyme-linked immunosorbent assay (ELISA) and fluke egg counts. Concurrent changes in peripheral blood leukocyte subpopulations, lymphocyte proliferation, and cytokine responses were measured. Relationships between fluke infection and immune responses were analyzed by using multivariable linear mixed-effect models. All calves from one farm showed evidence of exposure, while cohorts from the remaining two farms remained negative over the grazing season. A type 2 immune response was associated with exposure, with increased interleukin-4 (IL-4) production, IL-5 transcription, and eosinophilia. Suppression of parasite-specific peripheral blood mononuclear cell (PBMC) proliferation was evident, while decreased mitogen-stimulated gamma interferon (IFN-γ) production suggested immunomodulation, which was not restricted to parasite-specific responses. Our findings show that the global immune response is modulated toward a nonproliferative type 2 state following natural challenge withF. hepatica. This has implications in terms of the timing of the administration of vaccination programs and for host susceptibility to coinfecting pathogens.

scholarly journals A Transcriptomic and Proteomic Atlas of Obesity and Type 2 Diabetes in Cynomolgus Monkeys

2021 ◽  
Author(s):  
Xianglong Zhang ◽  
Ying Lei ◽  
Oliver Homann ◽  
Marina Stolina ◽  
Songli Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Immune Response ◽  
Nonhuman Primate ◽  
Metabolic Disorders ◽  
Healthy Controls ◽  
Adipose Tissues ◽  
Cynomolgus Monkeys ◽  
Single Cell Rna Sequencing

Obesity and type 2 diabetes (T2D) remain major global healthcare challenges and developing therapeutics necessitate using nonhuman primate models. Here, we present transcriptomic and proteomic analyses of all the major organs of cynomolgus monkeys with spontaneous obesity or T2D in comparison to healthy controls. Molecular changes occur predominantly in the adipose tissues of individuals with obesity, while extensive expression perturbations among T2D individuals are observed in many tissues, such as the liver, kidney, brain, and heart. Immune response-related pathways are upregulated in obesity and T2D, whereas metabolism and mitochondrial pathways are downregulated. Incorporating human single-cell RNA sequencing findings corroborates the role of macrophages and monocytes in obesity. Moreover, we highlight some potential therapeutic targets including SLC2A1 and PCSK1 in obesity as well as SLC30A8 and SLC2A2 in T2D. Our findings provide insights into tissue-specific molecular foundations of obesity and T2D and reveal the mechanistic links between these two metabolic disorders.

scholarly journals NK cell recruitment limits tissue damage during an enteric helminth infection

2019 ◽  
Vol 13 (2) ◽  
pp. 357-370 ◽  
Author(s):  
Maria E. Gentile ◽  
Yue Li ◽  
Amicha Robertson ◽  
Kathleen Shah ◽  
Ghislaine Fontes ◽  
...  
Keyword(s):  
Immune Response ◽  
Nk Cells ◽  
Helminth Infection ◽  
Nk Cell ◽  
Early Response ◽  
Cell Recruitment ◽  
Parasitic Helminths ◽  
Cxcr3 Expression ◽  
Type 2 Immune Response

AbstractParasitic helminths cause significant damage as they migrate through host tissues to complete their life cycle. While chronic helminth infections are characterized by a well-described Type 2 immune response, the early, tissue-invasive stages are not well understood. Here we investigate the immune pathways activated during the early stages of Heligmosomoides polygyrus bakeri (Hpb), a natural parasitic roundworm of mice. In contrast to the Type 2 immune response present at later stages of infection, a robust Type 1 immune signature including IFNg production was dominant at the time of parasite invasion and granuloma formation. This early response was associated with an accumulation of activated Natural Killer (NK) cells, with no increase of other innate lymphoid cell populations. Parabiosis and confocal microscopy studies indicated that NK cells were recruited from circulation to the small intestine, where they surrounded parasitic larvae. NK cell recruitment required IFNγ receptor signaling, but was independent of CXCR3 expression. The depletion of tissue-infiltrating NK cells altered neither worm burden nor parasite fitness, but increased vascular injury, suggesting a role for NK cells in mediating tissue protection. Together, these data identify an unexpected role for NK cells in promoting disease tolerance during the invasive stage of an enteric helminth infection.

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