Thinking that immune memory is an exclusive feature of adaptive immunity is a common mistake, and recent evidences strongly indicates that the innate branch of our immune system is just as able to react adaptively to repeated stimuli, displaying a de facto innate immune memory. The molecular mechanism behind the ability of innate immune cells to be "trained" to act differentially to occasional or sustained stimuli resides in epigenetic modifications that are induced by imprinting signals that alter subsequent immune responses. Since innate immune cells are pivotal in inflammatory homeostasis in periphery as well as in the central nervous system (CNS) where they are involved in the modulation of neuronal functions, Ann-Christin Weldeln and colleagues, addressed an important question: is innate immune memory is involved in neuropathological alterations?
More than 75% of autoimmune diseases display increased prevalence in women, and estrogens have been often pointed out as possible responsible due to their involvement in a rather wide number of physiological functions, including immune ones. However, to date, the role of estrogens in immune reactions, especially T-dependent ones, is still not well understood.
In animal research, a clean environment is often considered a mandatory condition to avoid collateral and unwanted stimuli that might interfere with the experimental condition a researcher is investigating. On the other hand, the immune system of these animals seems to remain stunned by the lack of immune challenges, some says, to the point that these animals might not represent a bona fide model for the immune system.
One of the hardest struggle in a scientist's life is writing a paper that is complete and compelling - yet concise, clear and, overall, understandable.
The concept of the brain as an "immune privileged" environment is fading away, as an ever growing number of papers is continuously demonstrating the strict functional connection between immunity and central nervous system.
Neuroimmunological modulation of host defense is emerging as a novel approach in enhancing immune response to pathogens, as the massive use of antibiotics is resulting in the increasing prevalence of drug-resistant strains of pathogens. As a matter of fact, lungs represent an important interface that is massively exposed to noxious bacterial stimuli and that must be constantly prone to avoid infection and microbial dissemination.
Neural stem cells (NSC) are emerging as a very promising new therapeutic tools in neurodegenerative diseases by virtue of their immuno-modulatory abilities; however the cellular and molecular mechanism that are behind their properties have not been fully elucidated yet. In this paper, published on Cell Stem Cell by Luca Perruzzotti-Jametti and colleagues, demonstrated that NSCs might reduce neuroinflammation by reducing succinate, which acts as an immunometabolite that is produced by pro-inflammatory myeolid phagocytes, during immune response, by triggering a plethora of inflammatory stimuli.
Spinal cord injury (SCI) is a devastating condition for which, to date, no effective clinical intervention has been found. Mesenchymal stem cells (MSCs) are emerging as possible cell-based therapy for many brain-related pathologies - including SCI - although the cellular and molecular mechanisms behind their effect are still quite unclear. In this paper, published on Scientific Reports, Katherine A. Ruppert and colleagues tried to administer MSC-derived endovescicles, which are thought to deliver paracrine regenerative factors, to rats undergoing spinal cord contusion.
Microbiota has been recently emerging as an unexpectedly important partner in immune homeostasis and its disfunctions have been correlated to virtually every immunopathological condition.
This year AINI has issued a generous numbers of Grants, both for the XXVII Congress of the Italian Association of Neuroimmuniology (AINI 2018 - Trieste, May 7-10, 2018) and the 14th International Congress of Neuroimmunology (ISNI 2018 - Brisbane - Australia, August 27-31, 2018).
The 1st Annual Scientific Meeting of the Italian Young Neuroscientists, BraYn (Brainstorming Research Assembly for Young Neuroscientists), which will be held in Genoa, Italy, during the 29th and 30th of June 2018, is inspired and organized by researchers under the age of 40 from different backgrounds and with different scientific approaches. The meeting aims establish connections between the future protagonists of Italian neuroscience.
BMAL1 gene is central in regulating circadian clock and rhythmic gene expression in mammal cells. However, its influence over physiological functions seems to be broader than expected, and it might be involved in unexpected pathways, including immune responses, since people displaying circadian disruptions are more prone to develop chronic inflammatory diseases.
Caroline E. Sutton and colleagues might have found the molecular machinery -or at least one of its important gears- of this mechanism, in this paper published on Nature Communication.
Low reproducibility is the greatest fear of every scientist, and, as a matter of fact, a plague in today's scientific research, with barely 40% of published data being considered reliably replicable.
In the last issue of Lancet Neurology, Jeffrey Alan Thompson (University College, London, UK), and its group, proposed an update of the McDonald criteria used to diagnose multiple sclerosis.
March 7-10, 2018
Bergamo - Bergamo Science Center
Il convegno è rivolto alla professione Medico Chirurgo, discipline: Neurologia e Allergologia e immunologia clinica, ed è accreditato ECM (18 crediti).
16 febbraio 2018
Aula Magna Giorgio De Sandre
POLICLINICO UNIVERSITARIO G.B. ROSSI - Verona
La multinazionale americana Pfizer frena sulla ricerca destinata alle patologie neurodegenerative e dirotta gli investimenti in aree in cui ha già raggiunto una forte leadership scientifica e il massimo impatto sui pazienti. Un disinvestimento da filoni importanti su Alzheimer e Parkinson che non hanno portato i frutti sperati, soprattutto nei tempi sperati. Lo ha dichiarato la stessa multinazionale, che ha anche annunciato un pesante impatto sul personale dedicato all’area delle demenze, con una riduzione totale dell’organico di circa 300 posizioni.
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Vaccines are, as a matter of fact, one of the greatest achievements ever obtained by human kind as they were able to eliminate infective diseases that, not too far in the past, were considered life-threatening menace or, quite often, a proper sentence to death. As a result, diseases such as tetanus or polio have become such a rare occurrence that, if on one hand the overall quality of life has improved significantly, on the other hand, the awareness of the perils represented by these infections (and the role played by vaccines in defeating them) has probably dwindled.
La Facoltà di Medicina e Chirurgia dell'Università di Modena e Reggio Emilia sta promuovendo degli incontri con gli studenti delle scuole medie superiori di Modena e Reggio Emilia sul tema delle vaccinazioni.
L'evento è patrocinato da AINI.
TNF receptors represent an important node of immune reactions, both innate and adaptive, and an important pharmacological target in the treatment of several autoimmune conditions. Their role has also been recently established in the regulation of Treg function, although the full extent and nature of the signals sprouting from the plethora of ligands that engage it is still poorly understood.
Mirela Kuka and Matteo Iannacone published last week a beautifully written review on B cells, their development, their interaction with viruses and the way cellular components of innate immunity can alter their function.
Published this month on Nature Reviews Immunology, this review represents an understandable and complete gathering of informations on the ontogenesis and involvement of CNS-resident microglia and peripheral macrophages in brain physiology and pathophysiology.
The transcription factor FoxP3 is endowed with the ability to repress conventional T cell phenotype while promoting Treg immunoregulatory properties by binding several specific sequences on the genome of T lymphocytes. However, understanding the mechanism by which this myriad of signals is coordinated in Tregs is no easy task, partly due to the fact that the signature genes targeted by FoxP3 represent only a small portion of the sequences actually recognized by this transcription factor on the whole genome; to make things harder, FoxP3 also directly interacts with a huge host of other different transcription factors. The integration of all these signals is behind Treg phenotype and is, to date, still poorly understood.