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how do macrophages have the capacity to digest pathogen in opsonization but not in the first time when the pathogen is new and they play the role of antigen presenting cells(APCs) first they digest polypeptide of antigen and then let the plasma cells first secrete an antibody and after that they can destroy antigens?

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  • $\begingroup$ There are multiple mechanisms to induce phagocytosis by macrophages. One includes B-cell antibodies (specifically the Fc region) and another includes chemokines emitted by local cells that can also induce phagocytosis. I do not have my material with me at the moment, but the short answer is: Macrophages can do both. They can eat pathogens without antibody stimulation, but antibodies can also stimulate them into action. $\endgroup$ – MCM Jan 18 '15 at 19:41
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It's a simple matter of ionic charge

Opsonization works because it is masking negative charge with positive charge. Phagocytosis works on positively charged things.

Your right though, the sequence seems odd.

  1. First something is phagocytosed (by a macrophage or another monocyte-derivative, these are the APCs... but neutrophils, which are not APCs or monocyte-derivates also perform phagocytosis but they dot not have the MHC-II to be described)
  2. then digested in endosome/lysosomal,
  3. then presented on the MHC class II,
  4. recognized by TCR on T-cell,
  5. then much more complicated stuff to get to B cells to convert to plasma cells
  6. plasma cells secrete the antibody, in order for opsonization of the pathogen to be phagocytosis more easily.

Yet it was the initial phagocytosis that led to this. A bit of a circle.

Here are three answers:

  • one is cytokines
  • another one is about how the TLR receptor mediates phagocytosis
  • a third is how complements act as opsonins

local presence of cytokines (ex. interleukins, interferon, TNF) from either innate or adaptive "immune system" (by "immune system" I mean immune cells other than macrophage, but also epithelium which secretes types of interferons) that lead to "signal transduction" ("signal transduction" is the intracellular chain reaction in response to the activation of the cytokine (or other ligand) binding to the receptor, too complicated for me to explain) that alters the behavior of macrophage to enhance phagocytosis.


On the other hand, PAMPs activate the TLR which could permit phagocytosis without prior activation from sources "other" than the thing being phagocytosis.

By "other" things I mean opsonins and cytokines.

PAMPs (pathogen associated molecular pattern) are things on the pathogen that are distinctively foreign to the host, like flagella or LPS [which is the outer membrane from gram (-) bacteria]

TLR is the receptor on the macrophage that recognizes PAMPs. I think that TLR simply enhances phagocytosis via signal transduction much like cytokines. As an interesting side note, the TLR is quite ancient in kingdom animalia, having it's origin in sponges as close to the beginning as you get). Other aspects of the immune system evolved later on specifically in vertebrate. In fact the lymphocytes is unique to jawed vertebrate (aka absent in agnathans and invertebrate) and i don't know much about antibody production in non-mammals. Also in lower vertebrate and invertebrate, phagocytosis is done by hemocytes. In other words, the TLR is pretty fundamental as far as immune stuff goes, more so than cell types doing their things (ex. plasma cell making antibodies, macrophages doing phagocytosis).


But there is also complement mediated opsonization, primarily C3b but other complement proteins as well. Finally there are yet more (less important) opsonins, Mannose-binding lectin and C-reactive protein (CRP). all of these things are "Acute phase reactants" that are secreted by the liver under inflammatory conditions, mediated by cytokines. Complement is not always activated by the immunoglobulins.

Complement is activated by

  1. classical pathway, again Fc region of antibody (IgG/IgM), just like antibody mediated opsonization. In addition, classical pathway can be activated by CRP binding to microbial polysaccharides

    1. alternative pathway, which is the spontaneous hydrolysis of C3. Under normal (non-infected) circumstances, this is normally prevented by a variety of mechanisms.

    2. activation by mannose binding lectin. MVL recognizes certain sugars that are found in certain positions that are unique to bacteria, fungi, viruses.

I'm saying all these things as explanations of human immune system. It's probably different in different animals, the more different the further away from human. The complement system has been discovered in primitive vertebrate (agnathans) and invertebrate (specifically in deuterostomes like protocordates and echinoderms) but there are variations.

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