Faculty Opinions recommendation of Aire deficient mice develop multiple features of APECED phenotype and show altered immune response.

2002 ◽  
Author(s):  
Jin-Xiong She
Keyword(s):  
Immune Response ◽  
Multiple Features ◽  
Altered Immune Response ◽  
Deficient Mice

scholarly journals Altered Immune Response and Implantation Failure in Progesterone-Induced Blocking Factor-Deficient Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Timea Csabai ◽  
Eva Pallinger ◽  
Arpad F. Kovacs ◽  
Eva Miko ◽  
Zoltan Bognar ◽  
...  
Keyword(s):  
Immune Response ◽  
Implantation Failure ◽  
Blocking Factor ◽  
Altered Immune Response ◽  
Deficient Mice

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.

scholarly journals IL-6 Is Not Absolutely Essential for the Development of a TH17 Immune Response after an Aerosol Infection with Mycobacterium tuberculosis H37rv

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 9
Author(s):  
Kristina Ritter ◽  
Jan Christian Sodenkamp ◽  
Alexandra Hölscher ◽  
Jochen Behrends ◽  
Christoph Hölscher
Keyword(s):  
Immune Response ◽  
Inflammatory Diseases ◽  
Mycobacterial Infection ◽  
Minor Effect ◽  
Mycobacterium Tuberculosis H37rv ◽  
Th 17 ◽  
Anti Inflammatory ◽  
A Minor ◽  
Aerosol Infection ◽  
Deficient Mice

Anti-inflammatory treatment of chronic inflammatory diseases often increases susceptibility to infectious diseases such as tuberculosis (TB). Since numerous chronic inflammatory and autoimmune diseases are mediated by interleukin (IL)-6-induced T helper (TH) 17 cells, a TH17-directed anti-inflammatory therapy may be preferable to an IL-12-dependent TH1 inhibition in order to avoid reactivation of latent infections. To assess, however, the risk of inhibition of IL-6-dependent TH17-mediated inflammation, we examined the TH17 immune response and the course of experimental TB in IL-6- and T-cell-specific gp130-deficient mice. Our study revealed that the absence of IL-6 or gp130 on T cells has only a minor effect on the development of antigen-specific TH1 and TH17 cells. Importantly, these gene-deficient mice were as capable as wild type mice to control mycobacterial infection. Together, in contrast to its key function for TH17 development in other inflammatory diseases, IL-6 plays an inferior role for the generation of TH17 immune responses during experimental TB.

Altered immune response in adult women exposed to diethylstilbestrol in utero

2001 ◽  
Vol 185 (1) ◽  
pp. 78-81 ◽  
Author(s):  
Louis Burke ◽  
Margot Segall-Blank ◽  
Carlos Lorenzo ◽  
Roselynn Dynesius-Trentham ◽  
David Trentham ◽  
...  
Keyword(s):  
Immune Response ◽  
In Utero ◽  
Adult Women ◽  
Altered Immune Response

Impact of Revaccinating Children Who Initially Received Measles Vaccine Before 10 Months of Age

PEDIATRICS ◽  
1986 ◽  
Vol 77 (4) ◽  
pp. 471-476
Author(s):  
Harrison C. Stetler ◽  
Walter A. Orenstein ◽  
Roger H. Bernier ◽  
Kenneth L. Herrmann ◽  
Barry Sirotkin ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Hemagglutination Inhibition ◽  
Cytopathic Effect ◽  
Neutralizing Antibody ◽  
Primary Vaccination ◽  
Measles Vaccine ◽  
Negative Study ◽  
Enzymelinked Immunosorbent Assay ◽  
Altered Immune Response

Two hundred fifty-four infants who had received measles vaccine at <10 months of age were revaccinated at ≥15 months of age, and their immune responses were compared with 129 control infants who received their first doses of measles vaccine at ≥15 months of age. Sera were collected at the time of revaccination (study infants) or primary vaccination (control infants), 3 weeks, and 8 months later and tested for antibody by hemagglutination inhibition (HI), enzymelinked immunosorbent assay (ELISA), and cytopathic effect neutralization (CPEN). Of the 121 study infants who were initially HI negative, 116 (95.9%) made HI antibody 3 weeks postrevaccination compared with 126 (99.2%) of 127 control infants (P = 0.19). Of the 63 study infants with no initial detectable antibody by any of the three tests, 14 (22.2%) had a measles-specific IgM response 3 weeks postrevaccination compared with 37 of 50 (74.0%) randomly chosen control infants. By 8 months after revaccination, the 121 initially HI-negative study infants were significantly less likely to have detectable HI antibodies than control infants (52.1% v 97.6%) (P < .001). However, 96.7% of these 121 study infants had detectable neutralizing antibody 8 months postrevaccination, an antibody thought to correlate best with protection. This study confirms the altered immune response to revaccination in infants first vaccinated prior to 10 months of age; however, the data suggest that most of these infants were successfully primed and are probably protected after revaccination.

scholarly journals The role of the immune response in the etiopathogenesis of endometriosis

2021 ◽  
Vol 68 (1) ◽  
pp. 40-47
Author(s):  
Catalina Diana Stanica ◽  
◽  
Adrian , Neacsu ◽  
Romina Marina Sima ◽  
Raluca Gabriela Ioan ◽  
...  
Keyword(s):  
Immune Response ◽  
Chronic Pelvic Pain ◽  
Economic Consequences ◽  
Reproductive Age ◽  
High Morbidity ◽  
Women Of Reproductive Age ◽  
Cytokines And Chemokines ◽  
Altered Immune Response

Endometriosis is a benign, chronic, estrogen-dependent condition, present in 10% of women of reproductive age. The condition is associated with chronic pelvic pain and infertility that influence their quality of life, as well as married life and has important socio-economic consequences. Despite its high morbidity, its etiopathogenesis is incompletely known. A large number of studies suggest that the ability of endometrial implants to grow in ectopic locations may be correlated with the altered immune response towards the endometriotic tissue. There are enough data to show that immune system mediators, such as cytokines and chemokines, are playing key roles in the onset and olso on progression of endometriosis. There are studies that prove the association between endometriosis and autoimmune diseases. The present paper aims to investigate the implications of the immune response in the etiopathogenesis of endometriosis. The study of cellular or humoral immunity deficits, the presence of autoantibodies associated with this condition, can facilitate the understanding of the mechanisms that lead to the appearance and spread of endometriosis. We hope that this information will ultimately provide the basis for the development of new effective approaches in endometriosis management.

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