article rediscovered cruising "my documents: What is Macrophage Inflammatory Protein-1 Alpha (MIP-1A)?
Human MIP-1A is a 8.0 kDa protein belonging to a small class of cytokines called chemokines. Chemokines are a large family of small molecular weight proteins that mediate recruitment of mononuclear cells both in vivo and in vitro, an important step in inflammatory response. (Clark et al., 1998) "There are four defined chemokine subfamilies based on their primary structure, CXC, CC, C and CX3C. The best characterized are the CC and CXC chemokines. Members of the CC chemokine subfamily, such as MCP-1, RANTES, MIP-1 Beta and MIP-1 Alpha are chemotactic for monocytes, subsets of lymphocytes and natural killer cells, whereas CXC chemokines generally, but not exclusively, induce neutrophil chemotaxis."
…Tony Moody of Duke Univ. School of Medicine used anti-lipid monoclonal antibodies taken from auto-immune disease patients, and confirmed that [in a test tube] the Anti-PS MABs “neutralized” virus, or decreased viral cell entry, and the mechanism was via release of cell-synthesized chemical attractant compounds called “chemokines.” The specific chemokines, called MIP1a and MIP1b, are chemicals secreted by monocytes, the white blood cell scavengers, which dock on, or attach to, cell membrane receptors (docking sites), plugging the port-hole in the cell membrane [receptor site] through which HIV enters a cell, That docking site is called the CCRF receptor. Moody found that “neutralization” of virus infection could be reversed by antibodies directed against the MIP1a and MIP1b, concluding that the MOA of anti-lipid antibodies is that they stick to the host target cell and not the virus to prevent infection. A vaccine that induces such antibodies may not be able to directly neutralize HIV but it may reduce virus spreading
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Tony Moody of Duke Univ. School of Medicine used anti-lipid monoclonal antibodies taken from patients with auto-immune disease, and confirmed that [in a test tube] the Anti-PS MABs “neutralized” virus, or decreased viral cell entry, and found that the probable mechanism was via release of cell-synthesized chemical attractant compounds called “chemokines.” Chemokines use chemical signals as attractants to other immune cells. The specific chemokines released by the antiPS MABs are called MIP1a and MIP1b, and are secreted by monocytes, the white blood cell scavengers. These chemoattractants dock on, or attach to, cell membrane receptors (docking sites), plugging the port-hole in the cell membrane [receptor site] through which HIV enters a cell, That docking site is called the CCRF5 receptor. Moody found that “neutralization” of virus infection could be reversed by antibodies directed against the MIP1a and MIP1b, concluding that the MOA of anti-lipid antibodies is that they stick to the host target cell and not the virus to prevent infection. A vaccine that induces such antibodies may not be able to directly neutralize HIV but it may reduce virus spreading
RA Chaurio published “Phospholipids: Key Players in Apoptosis and Immune Regulation, in which he said that “PS seems to be the major “eat me” signal and immune suppressor in the clearance process of apoptotic [normal death in] cells. He continues, “Since millions of cells die constantly in multicellular organisms and since there is a robust system for their rapid recognition and removal, this “silent clearance” of apoptotic cells is [somehow] associated with … impaired immunity and increased apoptosis. Cancer, exposure to irradiation, and some parasite and viral infections are considered to take advantage of this ubiquitous mechanism fostering disease development
