Review Literature on Inflammatory Reaction of Brain and Role of IL-33, IL-16, and CD4

Running head: REVIEW LITERATURE.
REVIEW LITERATURE
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1REVIEW LITERATURE
A growing body conclusively demonstrates that the inflammatory reaction of the
brain can be encouraged by Aβ plaques. The oligomeric form of the Aβ plaques applies
synaptotoxicity. Recently it was also discovered that the Aβ plaque could
initiate the cerebral amyloid angiopathy, which initiates the brain
hemorrhages and the vascular inflammation. Researches show that the
inflammatory processes such as dystrophic microglia, microgliosis, acute
phase protein change, cytokine elevation, astrocytosis and complement
activation can cause the accumulation of the Aβ plaques in parenchyma
and vasculature partially. The ageing and the compromised immune
system in elders can lead to the synthesis of the AD. The formation of the
AD as a result of allergic inflammation due to parasitic infection or any
other reaction and act as an alarming system to alert any immunity
compromise in the brain. Recent researches are aiming towards the
application of the usefulness of this phenomenon. The following
paragraphs will explain the features of the Aβ- reactive CD4 T cells in the
mammalian and other animal models and Aβ-based immunotherapeutic
methodologies for AD in situation to disease pathogenesis and
immunosenescence (Dembic 2015).
IL-33: an alarmin cytokine with crucial roles in innate immunity,
inflammation and allergy
This review is to high point the vital role of IL-33, and it’s mode of
action as an alarmin. IL-33 fit in to the IL-1 family, and it is a nuclear
cytokine mainly influences the epithelial barrier tissue and lymphoid
organs. It activates Myd-88 signalling pathways in the target cell showing

2REVIEW LITERATURE
the ST2/IL-IRAcP receptor complex. The IL-33 plays a crucial role in the
expression of the type-2 immunity. Studies show that IL-33 induces
allergic reactions as it produces IL-13 and IL-5 with the help of group 2
ILC2s cells like NK cells and mast cells, in the presence of microbial
infection. It acts as an alarm signal to alert cell (Arseniy, Yuzhalin, and
Kutikhin, 2015)
Il-33 is a nuclear cytokine which in the beginning selected as NF-
HEV. Which have similar structure with IL-1. Interleukin-33 frequently
detected as a nuclear protein. Past three years studies indicate that ILC2
secrets enormous amount of IL-13 and IL-5 in response to the IL-33. In
major researches in vivo It was found that These interleukin protein plays
essential role in the eosinophis homeostatis , type- 2 immunity and
allergic inflammations.
The neuropathology of the AD can be identified by the presence of
neurofibrillary tangles (NFTs) and abundant amyloid plaque (AP). This
results in hyperphosphorylated tau which leads to the loss of neurons. The
plaques contain activated microglia surrounded by the reactive
astrocytes. On the course of excess pathophysiological events, the IL-33
induces pro-inflammatory reactions and act as the mediator of
inflammation of the neurons in CNS. IL-33 activates the inflammatory cells
like glial cells. Various cytokines such as TNFα and IL-1β act as the
indicator in the AD patients. The IL-33 after cleavage with ST2 act as a
mature cytokine. Recent researches showed that IL-33 might heal the
central nervous system and other nervous system diseases (Xiong et al.
2014). This cytokine can be genetically linked with the human AD. Some