Conditioned Allergic Rhinitis: A Model For Central Nervous System And Immune System Interaction In Ige-Mediated Allergic Reactions

2019 ◽  
pp. 71-84
Author(s):  
M. Gauci ◽  
A.J. Husband ◽  
M.G. King
2017 ◽  
Vol 157 ◽  
pp. 71-82 ◽  
Author(s):  
Andrew M. Cowie ◽  
Kathleena I. Sarty ◽  
Angella Mercer ◽  
Jin Koh ◽  
Karen A. Kidd ◽  
...  

2018 ◽  
Vol 19 (12) ◽  
pp. 3856 ◽  
Author(s):  
Ivan Presta ◽  
Marco Vismara ◽  
Fabiana Novellino ◽  
Annalidia Donato ◽  
Paolo Zaffino ◽  
...  

Recent studies have clarified many still unknown aspects related to innate immunity and the blood-brain barrier relationship. They have also confirmed the close links between effector immune system cells, such as granulocytes, macrophages, microglia, natural killer cells and mast cells, and barrier functionality. The latter, in turn, is able to influence not only the entry of the cells of the immune system into the nervous tissue, but also their own activation. Interestingly, these two components and their interactions play a role of great importance not only in infectious diseases, but in almost all the pathologies of the central nervous system. In this paper, we review the main aspects in the field of vascular diseases (cerebral ischemia), of primitive and secondary neoplasms of Central Nervous System CNS, of CNS infectious diseases, of most common neurodegenerative diseases, in epilepsy and in demyelinating diseases (multiple sclerosis). Neuroinflammation phenomena are constantly present in all diseases; in every different pathological state, a variety of innate immunity cells responds to specific stimuli, differentiating their action, which can influence the blood-brain barrier permeability. This, in turn, undergoes anatomical and functional modifications, allowing the stabilization or the progression of the pathological processes.


2019 ◽  
Vol 26 (1) ◽  
Author(s):  
Alejandro Quintero-Villegas ◽  
Sergio Iván Valdés-Ferrer

AbstractIn mammalians, serotonin (5-HT) has critical roles in the central nervous system (CNS), including mood stability, pain tolerance, or sleep patterns. However, the vast majority of serotonin is produced by intestinal enterochromaffin cells of the gastrointestinal tract and circulating blood platelets, also acting outside of the CNS. Serotonin effects are mediated through its interaction with 5-HT receptors (5-HTRs), a superfamily with a repertoire of at least fourteen well-characterized members. 5-HT7 receptors are the last 5-HTR member to be identified, with well-defined functions in the nervous, gastrointestinal, and vascular systems. The effects of serotonin on the immune response are less well understood. Mast cells are known to produce serotonin, while T cells, dendritic cells, monocytes, macrophages and microglia express 5-HT7 receptor. Here, we review the known roles of 5-HT7 receptors in the immune system, as well as their potential therapeutic implication in inflammatory and immune-mediated disorders.


Physiology ◽  
2000 ◽  
Vol 15 (5) ◽  
pp. 250-255
Author(s):  
Michael A. Klein ◽  
Adriano Aguzzi

Prion diseases are fatal neurodegenerative disorders of animals and humans. Here we address the role of the immune system in the spread of prions from peripheral sites to the central nervous system and its potential relevance to iatrogenic prion disease.


2011 ◽  
Vol 18 (4) ◽  
pp. e62-e63 ◽  
Author(s):  
Lindsay Van Tongeren ◽  
Tawimas Shaipanich ◽  
John A Fleetham

A case ofCryptococcus gattii(pulmonary and central nervous system) andMycobacterium tuberculosis(pulmonary) coinfection in an otherwise healthy young woman is reported. The patient presented with a two-month history of dry cough. She had an unremarkable medical history. Both tuberculosis and cryptococcosis were diagnosed following bronchoscopy, and a subsequent lumbar puncture revealedC gattiiin the cerebrospinal fluid. There is evidence that bothM tuberculosisandC gattiimay have suppressive effects on the host immune system. This suggests a mechanism by which an otherwise healthy individual developed these two infections.


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