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Text
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<a href="http://doi.org/10.3389/fcimb.2020.00153" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fcimb.2020.00153</a>
Pages
153
Volume
10
ISSN
2235-2988 2235-2988
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Update Year & Number
June 2020 Update I
NEOMED College
NEOMED College of Medicine
NEOMED Department
NEOMED Student Publications
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Title
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The IL-33/ST2 Axis in Immune Responses Against Parasitic Disease: Potential Therapeutic Applications.
Publisher
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Frontiers in cellular and infection microbiology
Date
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2020
1905-07
Subject
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cytokine production; drug-resistance; endogenous il-33; IL-33; IL-33; immunity; inflammation; innate; innate lymphoid-cells; interleukin-33; mast-cells; parasite; receptor st2; ST2; ST2; tissue homeostasis; type-2 immunity
Creator
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Ryan Nathan; Anderson Kelvin; Volpedo Greta; Varikuti Sanjay; Satoskar Monika; Satoskar Sanika; Oghumu Steve
Description
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Parasitic infections pose a wide and varying threat globally, impacting over 25% of the global population with many more at risk of infection. These infections are comprised of, but not limited to, toxoplasmosis, malaria, leishmaniasis and any one of a wide variety of helminthic infections. While a great deal is understood about the adaptive immune response to each of these parasites, there remains a need to further elucidate the early innate immune response. Interleukin-33 is being revealed as one of the earliest players in the cytokine milieu responding to parasitic invasion, and as such has been given the name "alarmin." A nuclear cytokine, interleukin-33 is housed primarily within epithelial and fibroblastic tissues and is released upon cellular damage or death. Evidence has shown that interleukin-33 seems to play a crucial role in priming the immune system toward a strong T helper type 2 immune response, necessary in the clearance of some parasites, while disease exacerbating in the context of others. With the possibility of being a double-edged sword, a great deal remains to be seen in how interleukin-33 and its receptor ST2 are involved in the immune response different parasites elicit, and how those parasites may manipulate or evade this host mechanism. In this review article we compile the current cutting-edge research into the interleukin-33 response to toxoplasmosis, malaria, leishmania, and helminthic infection. Furthermore, we provide insight into directions interleukin-33 research may take in the future, potential immunotherapeutic applications of interleukin-33 modulation and how a better clarity of early innate immune system responses involving interleukin-33/ST2 signaling may be applied in development of much needed treatment options against parasitic invaders.
Identifier
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<a href="http://doi.org/10.3389/fcimb.2020.00153" target="_blank" rel="noreferrer noopener">10.3389/fcimb.2020.00153</a>
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journalArticle
2020
Anderson Kelvin
cytokine production
drug-resistance
endogenous il-33
Frontiers in cellular and infection microbiology
IL-33
Immunity
Inflammation
Innate
innate lymphoid-cells
interleukin-33
Journal Article
journalArticle
June 2020 Update I
mast-cells
NEOMED College of Medicine Student
NEOMED Student Publications
Oghumu Steve
parasite
receptor st2
Ryan Nathan
Satoskar Monika
Satoskar Sanika
ST2
tissue homeostasis
type-2 immunity
Varikuti Sanjay
Volpedo Greta