Protection relies only on the IL - 6 receptors that are bound
on macrophage cell membranes.
Not exact matches
By «plugging in» to the cardiomyocytes,
macrophages help the heart
cells receive the signals and stay
on beat.
By analyzing chemical changes of the IRS - 2 protein in immortalized cultures of human white blood
cells, it determined that IRS - 2 appeared in two different forms — «
on,» which allows the signal to pass through, and «off,» which stops the signal from activating the
cells into M2
macrophages.
In this study, the researchers found that a specific population of immune
cells called
macrophages have the ability to secrete or produce a protective or healing factor known as Interleukin - 10 (IL - 10), which can interact with receptors
on intestinal epithelial
cells to promote wound healing.
On encountering the TB bacillus, receptors on immune - system scavenger cells known as macrophages stimulate the conversion of circulating vitamin D to its active form, which produces a peptide that destroys the bacillu
On encountering the TB bacillus, receptors
on immune - system scavenger cells known as macrophages stimulate the conversion of circulating vitamin D to its active form, which produces a peptide that destroys the bacillu
on immune - system scavenger
cells known as
macrophages stimulate the conversion of circulating vitamin D to its active form, which produces a peptide that destroys the bacillus.
In mice with pancreatic tumors, Kalbasi and other members of the team found relatively high levels of inflammatory compounds including CCL2, the signaling molecule that activates CCR2
on monocytes and
macrophages to make these
cells migrate to tumors.
An early - stage clinical study by another institution, published in the Lancet Oncology in May 2016, combined chemotherapy with an experimental drug that blocks CCR2, a receptor
on monocytes and
macrophages whose activation stimulates these
cells to infiltrate tumors.
His group focused
on another type of immune
cell known as primary
macrophages and their response to live bacterial pathogens.
TLR7 is one of a family of receptors present
on innate immune
cells like
macrophages that have been linked to chronic inflammation and autoimmunity.
When looking for culprits, researchers have often focused their microscopes
on macrophages, which occupy a meaningful spot among the white blood
cells in the tumor microenvironment.
In 2010, it was discovered that enhancers directed expression of RNA
on a broad scale in neurons and
macrophages, a type of immune system
cell.
The new NYU Langone study revolves around the ability of immune
cells to «decide» which
cell types to become based
on the type of invader encountered — including
macrophages that arrive first at the sites of infection.
Antigen - presenting
cells (APCs), such as dendritic
cells and
macrophages, activate T
cells by engaging protein receptors
on the T
cell surface.
«These findings question a long - held paradigm that myelin - specific T
cells initiate inflammation in the brain through activation of microglia and brain
macrophages,» says Scott Zamvil, MD, PhD, a professor of neurology at the University of California, San Francisco and co-author
on the paper.
This activation causes additional stress which keeps the
macrophages «turned
on» in a cycle that amplifies and further damages the
cells and surrounding tissues.
When SIRPA contacts CD47
on any other
cell, it serves as a safeguard that prevents the
macrophage from engulfing the other
cell, even if it's cancerous.
«The big surprise,» Discher said, «is that injected
macrophages circulate all around the body but accumulate only within the tumors where they engorge
on cancer
cells.»
The Discher Lab has since shown that a protein
on human
cells called CD47 functions as a «marker of self» by interacting with a protein
on the surface of
macrophages called SIRPA.
The Discher lab has expertise with mimicking these protective mechanisms
on healthy
cells, but now they are targeting the proteins
on macrophages that respond to those signals.
Soon, dying muscle
cells and dying
macrophages join a growing plaque
on the artery wall.
On top of the T
cell abnormalities, chronic GVHD involves antibody - producing B
cells and scavenger
cells called
macrophages.
This relies
on the ability of
macrophages, types of white blood
cell, to produce nitric oxide when they are exposed to cytokines.
Once switched
on,
macrophages then decide whether immune
cells including natural killer
cells receive their marching orders,» explains Prof. Dr. Veit Hornung.
By means of their mouse model, the hormone researchers from Ulm could prove that dexamethasone — mediated through the dimer function of GR — leads to the release of sphingosine -1-phosphate in the
macrophages, a tissue hormone that fosters growth, migration and division of
cells and has a stabilization effect
on inner vessel walls.
The researchers focused
on how hematopoietic stem
cells developed into one of two types of white blood
cells:
macrophages or neutrophils.
«For instance, if you've got hepatitis B infection, then you're going to have impaired
macrophage function in the liver, which is going to impair the ability of those
cells to go
on and respond to other viruses.
Expression of C - type lectin, SIGNR3,
on subsets of dendritic
cells,
macrophages, and monocytes.
Skeletal muscle fiber formation, bone marrow stem
cell formation, thymus T -
cell formation, TNF - a / INF - gamma production by immune system's
macrophages (immunosenescence by IGF loss), neuregulin and brain - derived neutrophic factor depend
on IGF - 1 acting
on brain IGFR receptors.
The mechanism of action is based
on the activation of
macrophages to defend against tumors by direct tumor cytotoxicity and consequently they secrete cytokines which recruit secondary immune
cells, presenting antigen to T
cells [5 - 7].
Moreover, there are yet other
cell types — such as visceral adipose tissue
macrophages and cytotoxic CD8 + T -
cells — in which the age - related supernumerary accumulation of dysfunctional and apoptosis - resistant
cells appears to play a highly deleterious role
on tissue function, but where the
cells are not «senescent»
cells in the classical sense of p16Ink4a expression and the senescence - associated secretory profile observed in senescent fibroblasts.
Next steps: Future studies will focus
on investigation of 1) the biological functions of newly identified STM protein that is required for colonization of
macrophages and 2) Nramp1 - affected pathways in STM
cells.
Similarly, OX40L is inducible and has been found
on activated / mature APC such as dendritic
cells, B
cells, and
macrophages.
4 - 1BBL was largely thought to be
on APC that have been activated for several days, such as dendritic
cells, B
cells, and
macrophages although again it is clear that 4 - 1BBL is now more ubiquitous as it has been visualized to be induced
on diverse
cell types such as mast
cells, osteoclasts, smooth muscle, and stem
cells.
He has been interested in differentiation and growth control throughout his career and is an expert
on hematopoietic stem
cells,
macrophage differentiation, hematopoietic and Maf family transcription factors.
LIGHT can bind LTβR, a TNFR family molecule constitutively expressed
on stromal
cells, dendritic
cells,
macrophages, and some epithelial
cells.
The researchers focussed
on the ability of trehalose, a sugar consisting of two linked glucose molecules, to increase the amount of organelles inside specialized «housekeeping»
cells known as
macrophages.
In his research
on the axolotl, which is a Mexican salamander, Dr. Godwin discovered that when it comes to regenerating tissue without scarring, a white blood
cell called the
macrophage may be a triggering factor.
Whitehead Institute researchers have uncovered a novel association between two fungal recognition receptors
on the surface of certain immune
cells, called
macrophages.
Researchers focused
on white blood
cells called
macrophages that work to destroy invading bacterial microbes.
The researchers focused
on two types of white blood
cells, known as
macrophages and neutrophils.
Without Nr4a1 to put a damper
on production, monocytes and
macrophages increase secretion of norepinephrine, which in turn leads to the activation of
macrophages, thereby amplifying neuroinflammation and causing a massive influx of T
cells into the central nervous system.
When they used such mice to test their approach, they found that the bulk of therapeutic effect from CD47 blockade relied not
on macrophages but
on dendritic
cells.
They then showed that when activated, that DNA region, which they called «enhancer # 2» (E2), was capable of switching
on Nr4a1 expression only in patrolling monocytes, and not in related
cells like
macrophages.
The recent emphasis
on macrophages stems, in part, from promising, but problematic, efforts to develop an effective
macrophage - driven T
cell - mediated immunotherapy.
By changing the mouse model they use to study how the immune system responds to cancer, a team of researchers hopes to shift the focus for one form of cancer immunotherapy back to the standard approach — relying
on antigen - presenting dendritic
cells — and away from the current upstart,
macrophages.
Under the guidance of a world - renowned cancer biologist, Robert Weinberg, Ph.D., Lu is focusing
on how metastatic breast cancer
cells interact with a subset of immune
cells called
macrophages, which normally are capable of engulfing — literally eating — infected, damaged, or cancerous
cells.
His laboratories are focusing
on the ontogeny and differentiation of
macrophages and dendritic
cells (DCs).
The greater CD169 coating of Vγ4 + γδT
cells and their stronger dependence
on CD169 for retention in the SCS than the other innate - like lymphocytes suggests these
cells interact more strongly or in a more selective way with CD169 +
macrophages.
The
macrophages release cytokines that can activate more innate immune
cells, readying them for attack
on viruses or cancer
cells, or they can activate the adaptive arm of immunity, priming it for clonal expansion.
Because the damaged proteins
on the surfaces of tumor
cells look very different from healthy
cells, the immune system is alarmed, and natural killer (NK)
cells and
macrophages are immediately sent to the tumor.