Multiple sclerosis: an altered immune response or an altered stress response?

1996 ◽  
Vol 74 (6) ◽  
pp. 285-296 ◽  
Author(s):  
J. M. van Noort



Neurology ◽  
2004 ◽  
Vol 62 (12) ◽  
pp. 2277-2282 ◽  
Author(s):  
P. Sundstrom ◽  
P. Juto ◽  
G. Wadell ◽  
G. Hallmans ◽  
A. Svenningsson ◽  
...  


2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Maurice A. Canham ◽  
John D. M. Campbell ◽  
Joanne C. Mountford

Abstract More than seven months into the coronavirus disease -19 (COVID-19) pandemic, infection from the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has led to over 21.2 million cases and resulted in over 760,000 deaths worldwide so far. As a result, COVID-19 has changed all our lives as we battle to curtail the spread of the infection in the absence of specific therapies against coronaviruses and in anticipation of a proven safe and efficacious vaccine. Common with previous outbreaks of coronavirus infections, SARS and Middle East respiratory syndrome, COVID-19 can lead to acute respiratory distress syndrome (ARDS) that arises due to an imbalanced immune response. While several repurposed antiviral and host-response drugs are under examination as potential treatments, other novel therapeutics are also being explored to alleviate the effects on critically ill patients. The use of mesenchymal stromal cells (MSCs) for COVID-19 has become an attractive avenue down which almost 70 different clinical trial teams have ventured. Successfully trialled for the treatment of other conditions such as multiple sclerosis, osteoarthritis and graft versus host disease, MSCs possess both regenerative and immunomodulatory properties, the latter of which can be harnessed to reduce the severity and longevity of ARDS in patients under intensive care due to SARS-CoV-2 infection.



2001 ◽  
Vol 185 (1) ◽  
pp. 78-81 ◽  
Author(s):  
Louis Burke ◽  
Margot Segall-Blank ◽  
Carlos Lorenzo ◽  
Roselynn Dynesius-Trentham ◽  
David Trentham ◽  
...  


PEDIATRICS ◽  
1986 ◽  
Vol 77 (4) ◽  
pp. 471-476
Author(s):  
Harrison C. Stetler ◽  
Walter A. Orenstein ◽  
Roger H. Bernier ◽  
Kenneth L. Herrmann ◽  
Barry Sirotkin ◽  
...  

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.



MicroRNA ◽  
2021 ◽  
Vol 11 ◽  
Author(s):  
Geysson Javier Fernandez ◽  
Jorge Andrés Castillo ◽  
Diana Marcela Giraldo ◽  
Silvio Urcuqui-Inchima

Background: The pathogenesis associated with Dengue virus (DENV) infection is marked by the impairment of host immune response. Consequently, the modulation of immune response has emerged as an important therapeutic target for the control of DENV infection. Vitamin D has been shown to regulate the immune response in DENV infection, although the molecular mechanism remains poorly understood. Post-transcriptional regulation of mRNA by miRNAs offers an opportunity to gain insight into the immunomodulation mediated by vitamin D Objective: Previously, it has been observed that a high dose of vitamin D (4000 IU) decreased DENV-2 infection and inflammatory response in monocyte-derived macrophages (MDMs). Here, we examine whether high or low doses of vitamin D supplements exert differential effect on miRNA expression in DENV-infected macrophages Methods: We analyzed miRNA expression profiles in MDMs isolated from healthy individuals who were given either 1000 or 4000 IU/day of vitamin D for 10 days. MDMs before or after vitamin D supplementation were challenged with DENV-2, and miRNAs profiles were analyzed by qPCR arrays. Results: DENV-2 infected MDMs supplemented with 4000 IU, showed up-regulation of miR-374a-5p, miR-363-3p, miR-101-3p, miR-9-5p, miR-34a-5p, miR-200a-3p, and the family of miRNAs miR-21-5p, and miR-590-p. The miRNA profile and predicted target mRNAs suggested regulatory pathways in MDMs obtained from healthy donors who received higher doses of vitamin D. These DENV-2 infected MDMs expressed a unique set of miRNAs that target immune and cellular stress response genes. Conclusion: The results suggest vitamin D dose-dependent differential expression of miRNAs target key signaling pathways of the pathogenesis of dengue disease.



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