GcMAF   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 day!







Macrophage-specialized monocytes

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 distinguished
in connective tissue: Histiocyte
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., TNF-α, interferon-γ, 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 (inflammation)
Phagocytosis
Destruction of tumor cells
Removal of cell detritus
(obligate) antigen presentation
wound healing

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 response.

Antigen presentation
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 Cytokines.

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 tumor prevalence

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.