scholarly journals IL-2-secreting recombinant bacillus Calmette Guerin can overcome a Type 2 immune response and corticosteroid-induced immunosuppression to elicit a Type 1 immune response

2002 ◽  
Vol 14 (7) ◽  
pp. 793-800 ◽  
Author(s):  
S. L. Young
Keyword(s):  
Immune Response ◽  
Bacillus Calmette Guerin ◽  
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 Imiquimod Does not Affect Shedding of Viable Chlamydiae in a Murine Model ofChlamydia trachomatisGenital Tract Infection

2003 ◽  
Vol 11 (2) ◽  
pp. 81-87 ◽  
Author(s):  
Kyle H. Ramsey ◽  
Namir Shaba ◽  
Kevin P. Cohoon ◽  
Kevin A. Ault
Keyword(s):  
Immune Response ◽  
Murine Model ◽  
Antibody Responses ◽  
Igg Subclass ◽  
T Helper ◽  
Type 2 Immune Response ◽  
Significant Difference ◽  
Helper Type

Objective:We postulated that either oral or vaginal administration of the immune response modifier imiquimod would decrease vaginal shedding ofChlamydia trachomatis, mouse pneumonitis strain (MoPn), in a murine model.Methods:Female BALB/c mice were infected intravaginally withC. trachomatis(MoPn) and were administered imiquimod either orally (30 mg/kg) or vaginally (10 μl of 5%imiquimod cream) prior to infection and every second day after infection for a total of four doses. The course of infection was monitored by collecting cervical–vaginal swabs and isolation in HeLa 229 cell culture. To determine whether the drug affected T helper type 1 or T helper type 2 immune response polarization, immunoglobulinG(IgG) subclass antibody responses were assessed at day 56 after infection.Results:There was no significant difference in the course of infection when imiquimod-treated mice were compared with sham-treated controls, regardless of whether the drug was administered orally or vaginally. IgG subclass antibody responses, and by extension, T helper type 1 to T helper type 2 immune response polarization, were also unaffected.Conclusions:Imiquimod has no efficacy in controllingC. trachomatis(MoPn) infection in the murine model.

scholarly journals IL-4–producing B cells regulate T helper cell dichotomy in type 1- and type 2-controlled diseases

2017 ◽  
Vol 114 (40) ◽  
pp. E8430-E8439 ◽  
Author(s):  
Ramona Hurdayal ◽  
Hlumani H. Ndlovu ◽  
Mélanie Revaz-Breton ◽  
Suraj P. Parihar ◽  
Justin Komguep Nono ◽  
...  
Keyword(s):  
Immune Response ◽  
B Cells ◽  
B Cell ◽  
Cutaneous Leishmaniasis ◽  
Leishmania Major ◽  
Interleukin 4 ◽  
T Helper ◽  
Type 2 Immune Response

Interleukin-4 (IL-4)–induced T helper (Th) 2 cells promote susceptibility to the protozoan parasite Leishmania major, while conferring immunity to the intestinal trematode Schistosoma mansoni. Here, we report that abrogation of IL-4 receptor alpha (IL-4Rα) signaling on B cells in BALB/c mice (mb1creIL-4Rα–/lox) transformed nonhealer BALB/c to a healer phenotype with an early type 1 and dramatically reduced type 2 immune response and an absence of ulceration and necrosis during cutaneous leishmaniasis. From adoptive reconstitution and mixed bone-marrow chimera studies in B cell-deficient (µMT) mice, we reveal a central role for B cell-derived IL-4 and IL-4Rα in the optimal induction of the susceptible type 2 phenotype to L. major infection. We further demonstrate that the absence of IL-4Rα signaling on B cells exacerbated S. mansoni-induced mortality and pathology in BALB/c mice, due to a diminished type 2 immune response. In both disease models, IL-4Rα–responsive B cells displayed increased IL-4 production as early as day 1 after infection. Together, these results demonstrate that IL-4–producing and IL-4Rα–responsive B cells are critical in regulating and assisting early T helper dichotomy toward Th2 responses, which are detrimental in cutaneous leishmaniasis but beneficial in acute schistosomiasis.

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.

Endocrine autoimmunity

2011 ◽  
pp. 34-44 ◽  
Author(s):  
Matthew J. Simmonds ◽  
Stephen C. L. Gough
Keyword(s):  
Immune Response ◽  
Type 1 Diabetes ◽  
Immune System ◽  
Endocrine System ◽  
Graves Disease ◽  
Self Tolerance ◽  
Autoimmune Attack ◽  
Endocrine Organs

Dysfunction within the endocrine system can lead to a variety of diseases with autoimmune attack against individual components being some of the most common. Endocrine autoimmunity encompasses a spectrum of disorders including, e.g., common disorders such as type 1 diabetes, Graves’ disease, Hashimoto’s thyroiditis, and rarer disorders including Addison’s disease and the autoimmune polyendocrine syndromes type 1 (APS 1) and type 2 (APS 2) (see Table 1.6.1). Autoimmune attack within each of these diseases although aimed at different endocrine organs is caused by a breakdown in the immune system’s ability to distinguish between self and nonself antigens, leading to an immune response targeted at self tissues. Investigating the mechanisms behind this breakdown is vital to understand what has gone wrong and to determine the pathways against which therapeutics can be targeted. Before discussing how self-tolerance fails, we first have to understand how the immune system achieves self-tolerance.

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