Immune Response to Intracerebral Transplantation: Particular Properties of Stem Cells

2014 ◽  
pp. 169-189
Keyword(s):  
Stem Cells ◽  
Immune Response ◽  
Intracerebral Transplantation

scholarly journals Human Mesenchymal Stem Cells Exploit the Immune Response Mediating Chemokines to Impact the Phenotype of Glioblastoma

2012 ◽  
Vol 21 (7) ◽  
pp. 1529-1545 ◽  
Author(s):  
Helena Motaln ◽  
Kristina Gruden ◽  
Matjaž Hren ◽  
Christian Schichor ◽  
Monika Primon ◽  
...  
Keyword(s):  
Stem Cells ◽  
Immune Response ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells

Unexplored functions of sex hormones in glioblastoma cancer stem cells

Endocrinology ◽  
2022 ◽  
Author(s):  
Juyeun Lee ◽  
Katie Troike ◽  
R’ay Fodor ◽  
Justin D Lathia
Keyword(s):  
Stem Cells ◽  
Immune Response ◽  
Sex Differences ◽  
Cancer Stem Cells ◽  
Tumor Growth ◽  
Sex Hormones ◽  
Cellular Heterogeneity ◽  
Cellular Functions ◽  
Biological Sex ◽  
Organismal Development

Abstract Biological sex impacts a wide array of molecular and cellular functions that impact organismal development and can influence disease trajectory in a variety of pathophysiological states. In non-reproductive cancers, epidemiological sex differences have been observed in a series of tumors, and recent work has identified previously unappreciated sex differences in molecular genetics and immune response. However, the extent of these sex differences in terms of drivers of tumor growth and therapeutic response is less clear. In glioblastoma, the most common primary malignant brain tumor, there is a male bias in incidence and outcome, and key genetic and epigenetic differences, as well as differences in immune response driven by immune-suppressive myeloid populations, have recently been revealed. Glioblastoma is a prototypic tumor in which cellular heterogeneity is driven by populations of therapeutically resistant cancer stem cells (CSCs) that underlie tumor growth and recurrence. There is emerging evidence that GBM CSCs may show a sex difference, with male tumor cells showing enhanced self-renewal, but how sex differences impact CSC function is not clear. In this mini-review, we focus on how sex hormones may impact CSCs in GBM and implications for other cancers with a pronounced CSC population. We also explore opportunities to leverage new models to better understand the contribution of sex hormones versus sex chromosomes to CSC function. With the rising interest in sex differences in cancer, there is an immediate need to understand the extent to which sex differences impact tumor growth, including effects on CSC function.

scholarly journals The Regulation of the CNS Innate Immune Response Is Vital for the Restoration of Tissue Homeostasis (Repair) after Acute Brain Injury: A Brief Review

2010 ◽  
Vol 2010 ◽  
pp. 1-18 ◽  
Author(s):  
M. R. Griffiths ◽  
P. Gasque ◽  
J. W. Neal
Keyword(s):  
Stem Cells ◽  
Immune Response ◽  
T Cell ◽  
Innate Immune Response ◽  
T Cell Activation ◽  
Cell Activation ◽  
Tissue Homeostasis ◽  
Innate Immune ◽  
Apoptotic Cells ◽  
Treg Population

Neurons and glia respond to acute injury by participating in the CNS innate immune response. This involves the recognition and clearance of “not self ” pathogens and “altered self ” apoptotic cells. Phagocytic receptors (CD14, CD36, TLR–4) clear “not self” pathogens; neurons and glia express “death signals” to initiate apoptosis in T cells.The complement opsonins C1q, C3, and iC3b facilitate the clearance of apoptotic cells by interacting with CR3 and CR4 receptors. Apoptotic cells are also cleared by the scavenger receptors CD14, Prs-R, TREM expressed by glia. Serpins also expressed by glia counter the neurotoxic effects of thrombin and other systemic proteins that gain entry to the CNS following injury. Complement pathway and T cell activation are both regulated by complement regulatory proteins expressed by glia and neurons. CD200 and CD47 are NIRegs expressed by neurons as “don't eat me” signals and they inhibit microglial activity preventing host cell attack. Neural stem cells regulate T cell activation, increase the Treg population, and suppress proinflammatory cytokine expression. Stem cells also interact with the chemoattractants C3a, C5a, SDF-1, and thrombin to promote stem cell migration into damaged tissue to support tissue homeostasis.

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