Borgeson said one of lipoxin A4's key mechanisms of action is to switch the phenotype of the fat tissue
macrophage cells from inflammatory to anti-inflammatory.
«When we analyzed tissue samples in the lab, we found that exposing white fat to
macrophage cells from the immune system inhibited the transformation.»
Not exact matches
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.
[Chinedu Nwokoro et al., «Inhaled black carbon in the lower airways of London cyclists»] Researchers at the London School of Medicine collected sputum samples
from healthy non-smokers who walk or bike to see how much black carbon was in airway
macrophages — a type of white blood
cell that takes in foreign material.
The research team, Heller says, has already begun experiments to further explore the implications of these results, which include looking at differences in this pathway between
cells taken
from allergic and healthy individuals, and testing the efficacy of an inhalable drug that mimics the function of GRB1 and p70S6K to shut off the development of M2
macrophages in the lungs of mice.
Kilian said these questions range
from the basic — how
macrophages signal to the breast
cells — to the more long - term: Can therapeutics be used to disrupt that communication?
A final series of tests confirmed that toxic compounds generated by antibodies kill bacteria without any help
from other immune
cells, like
macrophages.
They have discovered that «itaconate» — a molecule derived
from glucose — acts as a powerful off - switch for
macrophages, which are the
cells in the immune system that lie at the heart of many inflammatory diseases including arthritis, inflammatory bowel disease and heart disease.
This is important as one of the reasons tumour
cells are so pernicious is that they are able to hide
from the body's immune system, by hijacking
macrophages.
Over the following few weeks, these
cells are replaced by new
macrophages derived
from precursor
cells known as monocytes.
In some instances, however, the flu virus can prevent the
macrophages from carrying out their protective function, allowing the epithelial
cells to become vulnerable to infection.
This study looked at two kinds of directly converted
cells: liver
cells made
from skin
cells, and
macrophages made
from B
cells.
The researchers used a new
cell tracing method to follow the movement of peritubular
macrophages from the bone marrow to the testes.
A combination of hypoxia and messages
from the tumor
cells initiates a process whereby the newly arrived
macrophages assume their bad - boy identity as tumor promoters.
Its analgesic effect stems
from the compound's ability to inhibit the production of cytokines and chemokines, which are small signaling molecules that attract inflammatory
macrophages to the nerve
cells.
Trapnell and Suzuki were prompted to test the novel
macrophage transplantation therapy by studies showing that resident
macrophage populations (such as those residing in the lung) can self - maintain without the
cells having to regenerate directly
from the bone marrow.
Pancreatic cancer
cells are known to emit signals that shift the lineage of in - rushing
macrophages from M1 to immune - suppressing M2.
Their interaction prevented first - responder immune
cells, called
macrophages,
from triggering reactions that kill cancer
cells.
When mice bearing pancreatic tumors were injected with an antibody that prevents galectin - 9
from docking into dectin - 1, they developed M1
macrophages, which sent signals that dramatically increased the number of T
cells capable of attacking the cancer
cells.
Copeland's team also noted that these mice suffered
from a host of immune - related problems, the most crippling being a flood of
macrophages — a type of white blood
cell — damaging the lungs and other organs.
Mammals keep iron out of reach of invading microbes by storing it in
cells like
macrophages — white blood
cells which, among other things, normally «recycle» the iron
from red blood
cells back into the bloodstream.
The study examined nanoparticle entry into endothelial
cells and
macrophages for the in vitro study, and the same type of
cells from the lung, heart and bone marrow for the in vivo component.
Drs. Merad and Mortha are now developing a multiscale approach to identify GM - CSF downstream targets using
macrophages and dendritic
cells isolated
from GM - CSF deficient mice and exposed to recombinant GMCSF.
They will study human
macrophages and dendritic
cells isolated
from IBD patients with defective GM - CSF function, «The approach represents a step forward in personalizing how we treat patients with IBD,» said Dr. Colombel.
Their idea emerged
from test - tube experiments that Munn did years ago, when he showed that some
macrophages could stop T
cells in their tracks by starving them of a building block called tryptophan.
Her research suggested that T
cells can also send signals that activate the brain's resident immune
cells, microglia and blood - borne
macrophages, telling them to protect the injured neurons
from toxins released by the injury.
By inhibiting the COX - 2 enzyme, and consequently inhibiting interleukin - 17A, celecoxib could indirectly prevent
macrophages from killing the injected stem
cells and instead allow them to heal the wound.
It is now understood that such
macrophages received the same «don't eat me» signal
from both healthy and cancerous
cells.
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.
«Safety thus far is likely a consequence of both the relatively small number of engineered
macrophages that are injected and their sequestration into the tumors, away
from most healthy
cells,» Discher said.
«Our new approach takes young and aggressive
macrophages from the bone marrow of a human donor and removes a key safeguard that cancer
cells have co-opted to prevent them
from being engulfed,» Alvey said.
CD47 is key to protecting red blood
cells from macrophages, and red blood
cells are particularly sensitive to the blocking effects of the antibody as they get older, Leeper says.
In this study, the researchers found that
macrophages from mice lacking Smurf1 were unable to attach the death - tagging protein ubiquitin to intracellular bacteria, resulting in a failure of the autophagy pathway and runaway growth of the bacteria inside the
cells.
Dr. Barreiro's team demonstrated how the protective programs were imprinted and transmitted
from stem
cells all the way to
macrophages.
So Christina Cammel of the Yale School of Medicine and her team isolated
macrophages from the fat tissue of young and old mice, and sequenced the DNA
from these
cells.
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.
In a separate set of experiments, Frank showed that the PcrV antibodies prevented the bacterium
from shooting its toxin into
cells, including
macrophages, the immune system's scavenger
cells, which are particularly vulnerable to Pseudomonas.
To test whether adipose tissue F4 / 80 +
cells shared a common bone marrow origin with other tissue
macrophage populations, we transplanted bone marrow
from C57BL / 6J mice expressing the CD45.1 leukocyte marker into 6 - week - old lethally irradiated C57BL / 6J mice expressing the CD45.2 leukocyte marker.
The bacteria hide within human
cells called
macrophages, escaping the body's own immune defenses and being shielded
from many types of antibiotics.
Macrophages stained with F4 / 80 - APC were separated
from F4 / 80 —
cells using a FACSAria
cell sorter (BD Biosciences Immunocytometry Systems Inc., San Jose, California, USA).
Dr Vince said that soon after infecting a
macrophage, Legionella bacteria alter the composition of proteins within their host
cell to prevent the host
from detecting the infection.
Expression analysis of
macrophage and nonmacrophage
cell populations isolated
from adipose tissue showed that adipose tissue
macrophages are the primary sources of TNF - α and other proinflammatory molecules in adipose tissue.
In response to this damage, immune
cells residing in the liver are activated, especially
macrophages, and additional immune
cells are recruited
from the circulating blood.
Immunohistochemical detection of
cells expressing the
macrophage - specific antigen F4 / 80 (arrows) in extensor digitalis longus muscles
from C57BL / 6J (a and c) Lepob / ob female and (b and d) lean female mice.
If ingested, the fungal
cells resist digestion while hiding
from antibodies, T
cells, and other immune system components, effectively converting a
macrophage into a microbial Trojan horse.
To determine whether adipose tissue
macrophages express any molecules implicated in obesity - associated complications, we isolated three
cell populations
from the parametrial adipose tissue of three obese B6.V Lepob / ob mice: (a) an adipocyte - enriched population, (b) a stromal vascular
macrophage F4 / 80 + population, and (c) an F4 / 80 — stromal vascular population.
Flow cytometry of SVCs isolated
from two perigondadal adipose tissue depot illustrates that tissue
from macrophage - deficient mice (b) contains 34 % the number of F4 / 80 +
cells found in adipose tissue
from control mice (a).
Macatonia SE, Hsieh C - S, Murphy KM, O'Garra A. Dendritic
cells and
macrophages are required for Th1 development of CD4 + T
cells from alpha beta TCR transgenic mice IL - 12 substitution for
macrophages to stimulate IFN - gamma production is IFN - gammadependent.
Resident
macrophages from the same lineage, such as liver Kupffer
cells, brain microglia, epidermal Langerhans
cells, lung alveolar
macrophages..., display tissue - specific phenotypes, perform tissue - specific functions and have distinct gene expression profiles.
To illuminate the mechanisms behind this observation, they treated
macrophages from both mice and humans with dimethyl itaconate, which is a version of itaconate that makes it easier to permeate through the
cells» membrane.