scholarly journals Immunization of BALB/c Mice with Killed Neospora caninum Tachyzoite Antigen Induces a Type 2 Immune Response and Exacerbates Encephalitis and Neurological Disease

2000 ◽  
Vol 7 (6) ◽  
pp. 893-898 ◽  
Author(s):  
Timothy V. Baszler ◽  
Terry F. McElwain ◽  
Bruce A. Mathison
Keyword(s):  
Immune Response ◽  
Neurological Disease ◽  
Neospora Caninum ◽  
Brain Lesions ◽  
Lymphoid Cells ◽  
Interleukin 4 ◽  
Type 2 Immune Response ◽  
Parasite Challenge

ABSTRACT BALB/c mice were immunized subcutaneously with solubleNeospora caninum tachyzoite antigen (NSO) entrapped in nonionic surfactant vesicles (NISVs) or administered with Freund's complete adjuvant (FCA). Following virulent parasite challenge, groups of mice immunized with NSO and either NISVs or FCA had clinical neurological disease and increased numbers of brain lesions compared to groups of mice inoculated with FCA, NISVs, or phosphate-buffered saline (PBS) alone. Increased numbers of brain lesions were statistically significant only between mice immunized with NISV-NSO and NISV- or PBS-treated mice. Following parasite challenge, brain inflammatory infiltrates in all experimental and control groups of mice were relatively similar and consisted of compact infiltrates of macrophages admixed with various numbers of lymphoid cells. Increased brain lesions in NSO-immunized mice were associated with increased antigen-specific interleukin 4 (IL-4) secretion and increased IL-4:gamma interferon secretion ratios from splenocytes in vitro and increased antigen-specific immunoglobulin G1 (IgG1):IgG2a ratios in vivo. Thus, immunization with whole killed N. caninum antigen and either liposoidal or Freund's adjuvant induced a type 2 immune response that was associated with worsened disease. The present studies emphasize the need to identify specific N. caninum antigens or other delivery systems that will elicit protective immune responses to neosporosis.

scholarly journals In chronic pancreatitis CD25+/Foxp3+ regulatory T-cells control pancreatic fibrosis by suppression of the type 2 immune response

2021 ◽  
Author(s):  
Juliane Glaubitz ◽  
Anika Wilden ◽  
Janine Golchert ◽  
Georg Homuth ◽  
Uwe Voelker ◽  
...  
Keyword(s):  
Immune Response ◽  
Chronic Pancreatitis ◽  
Disease Onset ◽  
Pancreatic Tissue ◽  
Lymphoid Cells ◽  
T Helper ◽  
Exocrine Insufficiency ◽  
Tissue Replacement ◽  
Type 2 Immune Response

Abstract Chronic pancreatitis (CP) is characterized by chronic inflammation and the progressive fibrotic replacement of exocrine and endocrine pancreatic tissue. We identified Tregs as central regulators of the fibroinflammatory reaction by a selective depletion of Foxp3-positive cells in a transgenic mouse model (DEREG-mice) of experimental CP. In Treg-depleted DEREG-mice, the induction of CP resulted in a significantly increased stroma deposition, the development of exocrine insufficiency and significant weight loss starting from day 14 after disease onset. In CP, Foxp3+/CD25+ Tregs suppress the type-2 immune response by a repression of Gata3+ T-helper cells (Th2), Gata3+ innate lymphoid cells type 2 (ILC2) and CD206+ M2-macrophages. A suspected pathomechanism behind the fibrotic tissue replacement may involve an observed dysbalance of Activin A expression in macrophages and of its counter regulator Follistatin. Our study identified Tregs as key regulators of the type-2 immune response and of organ remodeling during CP. The Treg-triggered immune response could be a therapeutic target to prevent fibrosis and preserve functional pancreatic tissue.

Clinical implication of detecting sensitization to iodinated radiocontrast media in the basophil activation test by flow cytometry

2021 ◽  
Vol 66 (12) ◽  
pp. 747-754
Author(s):  
N. V. Bychkova ◽  
P. A. Selivanov ◽  
N. M. Kalinina
Keyword(s):  
Flow Cytometry ◽  
Immune Response ◽  
T Lymphocytes ◽  
Basophil Activation Test ◽  
Basophil Activation ◽  
Activation Test ◽  
Radiocontrast Media ◽  
Type 2 Immune Response

The use of iodinated radiocontrast media is necessary for visualization. A number of patients have adverse effects of various nature and severity when these drugs are administered. Routine allergy tests do not provide adequate diagnosis of reactions to drugs in this group. The aim of this work is to assess the capabilities of the basophil activation test to confirm sensitization to non-ionic iodinated radiocontrast media, as well as to select a safe alternative drug in patients with a burdened history. Basophil activation test by flow cytometry was performed in 184 patients The Nikiforov Russian Centre of Emergency and Radiation Medicine» EMERCOM of Russia and 32 volunteers using ultravist, omnipack, and optiray. The presence of sensitization was assessed based on the basophil activation index, as well as spontaneous and anti-IgE antibody-induced activation of basophils and the population of T-lymphocytes type 2 immune response. The volunteers showed no sensitization to iodinated radiocontrast media. In patients with a medium degree of hypersensitivity reaction in vivo, in vitro sensitization to drugs was detected 4 times more often than in patients with a mild degree (51% versus 13.5%). In patients with systemic reactions to the administration of a known drug, in vitro sensitization was confirmed in 86% of cases, while the frequency of detection of sensitization to drugs did not differ. Spontaneous activation of basophils in patients and type 2 T-lymphocytes were 2 times higher than in volunteers. Patients were more likely to have low (less than 30%) activation of basophils for anti-IgE antibodies. The specificity of the basophil activation test with iodinated radiocontrast media was 100% with a sensitivity of 94.1%. Most patients were able to select a non-sensitizing contrast. Inclusion in the algorithm of spontaneous and anti-IgE antibody-induced activation of basophils and a population of T-lymphocytes type 2 immune response will allow the doctor to carry out a personalized approach to the management of patients with a burdened history.

scholarly journals C57BL/6 Mice Infected with Neospora caninum During Administration of Progesterone Show Bias Toward Type 2 Immune Response

2007 ◽  
Vol 69 (10) ◽  
pp. 1095-1097 ◽  
Author(s):  
Rika KANO ◽  
Akimasa KUDO ◽  
Hikaru KAMIYA ◽  
Yoshiyasu KOBAYASHI ◽  
Ryuichiro MAEDA ◽  
...  
Keyword(s):  
Immune Response ◽  
Neospora Caninum ◽  
Type 2 Immune Response

scholarly journals Group 2 Innate Lymphoid Cells: A Double-Edged Sword in Cancer?

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3452
Author(s):  
Enrico Maggi ◽  
Irene Veneziani ◽  
Lorenzo Moretta ◽  
Lorenzo Cosmi ◽  
Francesco Annunziato
Keyword(s):  
Immune Response ◽  
Inflammatory Responses ◽  
Cell Subset ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Th2 Cell ◽  
Type 2 Immune Response ◽  
Group 2 ◽  
Lymphoid Organogenesis

Group 2 Innate Lymphoid Cells (ILC2s) belong to the family of helper ILCs which provide host defense against infectious agents, participate in inflammatory responses and mediate lymphoid organogenesis and tissue repair, mainly at the skin and mucosal level. Based on their transcriptional, phenotypic and functional profile, ILC2s mirror the features of the adaptive CD4+ Th2 cell subset, both contributing to the so-called type 2 immune response. Similar to other ILCs, ILC2s are rapidly activated by signals deriving from tissue and/or other tissue-resident immune cells. The biologic activity of ILCs needs to be tightly regulated in order to prevent them from contributing to severe inflammation and damage in several organs. Indeed, ILC2s display both enhancing and regulatory roles in several pathophysiological conditions, including tumors. In this review, we summarize the actual knowledge about ILC2s ability to induce or impair a protective immune response, their pro- or antitumor activity in murine models, human (children and adults) pathologies and the potential strategies to improve cancer immunotherapy by exploiting the features of ILC2s.

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.

scholarly journals Maintenance of Type 2 Response by CXCR6-Deficient ILC2 in Papain-Induced Lung Inflammation

2019 ◽  
Vol 20 (21) ◽  
pp. 5493 ◽  
Author(s):  
Meunier ◽  
Chea ◽  
Garrido ◽  
Perchet ◽  
Petit ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Nk Cell ◽  
Lymphoid Cells ◽  
Inflammatory Conditions ◽  
Airway Diseases ◽  
Type 2 Cytokines ◽  
Lymphoid Organogenesis ◽  
Deficient Mice

Innate lymphoid cells (ILC) are important players of early immune defenses in situations like lymphoid organogenesis or in case of immune response to inflammation, infection and cancer. Th1 and Th2 antagonism is crucial for the regulation of immune responses, however mechanisms are still unclear for ILC functions. ILC2 and NK cells were reported to be both involved in allergic airway diseases and were shown to be able to interplay in the regulation of the immune response. CXCR6 is a common chemokine receptor expressed by all ILC, and its deficiency affects ILC2 and ILC1/NK cell numbers and functions in lungs in both steady-state and inflammatory conditions. We determined that the absence of a specific ILC2 KLRG1+ST2– subset in CXCR6-deficient mice is probably dependent on CXCR6 for its recruitment to the lung under inflammation. We show that despite their decreased numbers, lung CXCR6-deficient ILC2 are even more activated cells producing large amount of type 2 cytokines that could drive eosinophilia. This is strongly associated to the decrease of the lung Th1 response in CXCR6-deficient mice.

Su.77. Immune Response to T-independent Antigen Type 2 in vitro

2008 ◽  
Vol 127 ◽  
pp. S149
Author(s):  
Ekaterina Sidorova ◽  
Marina Gavrilova ◽  
Irina Chernyshova
Keyword(s):  
Immune Response
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