A new possibility of Treatment GCMAF is not an oncological substance
such as chemotherapy or the latest antibody therapies.
What does GCMAF do? As its name suggests, GCMAF is a macrophage-stimulating molecule. It
activates the formation of macrophages as well as reminds the macrophages of
their original tasks.
What are you doing with the GCMAF
in Effect, we restart the body's "underlying immune response" by
adding the GCMAF molecule. Thus, e.g. the tumor tissue is no longer able to
isolate itself. The tumor cell can`t block further on invading medicines.
Looking at the function of different macrophages, we can understand their
efficiency in the field of neurobiological diseases.
Although the Efficiency in case of the so called Mucous event Leaky Gut
Because we have different macrophages, floating, tissue and organ-specific
macrophages, the different areas of application are explained. The lifetime of
the macrophages explains the injection intervals, each 3rd - 6th
from ancient Greek:
"makrós" - big and "phagein" - food
Macrophages are large, mobile, mononuclear cells that are part of the cellular
immune system. They develop from circulating peripheral blood Monocytes, which
have a half-life of about 72 hours. Monocytes
can migrate into the tissue and remain
there for several weeks to months as tissue macrophages.
Macrophages develop from the Monocytes, formed in the bone marrow. These cells
are flushed out into the blood vessels and circulate in the blood stream.
During infection, they are attracted to the site of infection by Chemotaxis and
differentiate into Macrophages under the
influence of cytokines and antigens in the tissue. They can be activated,
for example, by IL-1 or by interferon-gamma.
A distinction is made between site-independent, mobile macrophages that migrate from the blood as needed and local, specific tissue macrophages,
which make up the majority of the macrophage population. The tissue macrophages are bound to a specific tissue and differ in
their morphology. Thus, the following macrophages are to be
in connective tissue:
in the brain: Microglia Cell
in the lungs: alveolar Macrophages
in the liver: Kupffer's star Cell
in the placenta: Hofbauer Cell
in the bone: Osteoclast
in skin: Langerhans cell
M1 phenotype Endotoxins such as lipopolysaccharides (LPS) or proinflammatory cytokines (e.g.,
etc.) cause the formation of a highly proinflammatory macrophage phenotype, the
so-called M1 phenotype. This is characterized
by a production of the enzyme iNOS (inducible NO synthase) and the consecutive
formation of NO radicals, which have a strong cytotoxic effect on surrounding
cells. Furthermore, this phenotype also releases proinflammatory cytokines to
initiate an immune response, e.g. in response to pathogens, but also after
tissue injury to "clean up" the occurring cellular debris. M2 phenotype
Anti-inflammatory cytokines such as IL-4 or tissue desbris, e.g. Myelin following peripheral nerve injury
induces an anti-inflammatory M2 phenotype with high phagocytic capacity. In the
context of tissue regeneration, this phenotype is often referred to as
"pre-regenerative" because it both stimulates stem cell
differentiation and secretes growth factors and anti-inflammatory cytokines
that result in proliferation of the corresponding cells in the tissue. The
M2 phenotype also frequently exists in tumors: Almost all solid tissue tumors
are characterized by high expression of M2 marker proteins, such as e.g.
Arginase 1 (Arg-1). The anti-inflammatory M2 macrophages are thought to
contribute to Immun Suppression in the tumor microenvironment and thereby to
the immune evasion and growth of tumors tasks.
As part of the Mononuclear- Phagocytic system (MPS), the Macrophages have
variety functions within the framework
of the pathogen defense:
central role in the initiation and regulation of defense reactions
Destruction of tumor cells
Removal of cell detritus
(obligate) antigen presentation
Phagocytosis Macrophages recognize pathogenic pathogens via so-called pattern
recognition receptors, e.g. the TLR. Their most important task is the
phagocytosis of microorganisms and other foreign bodies in the context of
nonspecific defense. The cytoplasm of macrophages contains a large number of
Lysosomes containing Lytic Enzymes that kill phagocytic pathogens. This process
leads to the so-called "activation" of the macrophage, and
subsequently to the secretion of cytokines that control the inflammatory
Macrophages process phagocytosed pathogens into peptide fragments that they
present to the cell surface with the help of MHC II molecules. The antigen
complexes are recognized by T helper cells, and start producing specific
antibodies. Release of cytokines Contact with pathogens via a PRR (Pattern Recognition Receptor) activates Macrophages.
This results in: release of various cytokines and pro-inflammatory factors such
as IL-1β, IL-2, IL-6 and TNF-α. The presence of zinc
can increase this effect. Zinc can increase this effect until fever. To prevent
an uncontrolled immune response, Macrophages also secrete anti-inflammatory
Cytokines such as IL-10. Muscle recovery Non-phagocytic macrophages play an important role in the repair of damaged
muscle fibers. Presumably by the secretion of proteins, proliferation and
differentiation of muscle cells is controlled. Nerve Regeneration Macrophages are active in the context of peripheral nerve regeneration. In
the first phase after a nerve injury, especially M1 macrophages are active,
which stimulate the immune system to break down the degenerating nerve stump.
In the further course, dominant M2 macrophages Phagocytose Myelin and dead Cells
and contribute to the differentiation of Schwann- Cells through the release of
Immunization by virus propagation
In the spleen, CD169-positive macrophages play a key role in viral infections
in generating enough virus particles to induce an immune response. So, to speak
about "Incubation", whereby the Differentiation and Multiplication of
the lymphocytes is stimulated.
What changes in this system with
Cancer Immune blocking: Monocytes and Macrophage Therapy
Cancer cells enter the immune brake, for example, NAGALASE is one of these
Substances, which blocks the Immunreaction.
For cancer cells to spread and multiply successfully, they must find a way to
escape the body's defenses.
Scientists at the German Cancer Research Center (DKFZ) are now publishing an
explanation, how this works in chronic lymphocytic leukemia (CLL).
• The degenerate cells trigger an inflammatory response and thereby affect
other blood cells in such a way that the immune defense is throttled.
To do this, they send out messages about Exosomes, small bubbles that release
cells into the environment. The discovery of the DKFZ researchers paves the way
for new therapeutic approaches.
Tumor cells affect their environment to escape the body's immune response and provide
favorable growth conditions.
Niels Halma of the DKFZ explained: .....
Some tumors succeed in activating precisely this macrophage protection for
themselves. This happens because the macrophages seem to misinterpret a signal
from other immune cells, namely the cry for help of exhausted T cells:
"In principle, they are so exhausted from the ongoing fight against the
tumor cells that they send a messenger substance that is supposed to cause more
of these T cells to come and act against the tumor. But in this situation, the
signal causes the macrophage to say, 'Here, make sure you protect the tissue,'
so it protects the tumor. "
In short, T cells signal the wrong thing to macrophages in tumor tissue. Niels
Halama went in search of drugs that might catch that signal. He found what he
was looking for in AIDS therapy.
For solid tumors, ie those that grow as a solid tissue in an organ, it has long
been known that they manipulate macrophages, the phagocytes of the immune
system, for your purposes.