anciendaze
Senior Member
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@Chriswolf
Lymphocyte infiltration of salivary glands is fairly common, even in people without ME/CFS. There are many possible causes, like infection by CMV, and the type of lymphocyte gives a clue as to what those cells "think" they are attacking. Endothelial dysfunction also takes place in many cases labeled ME/CFS, and even T-cell infiltration of endocrine organs and some nerve ganglia. If this resulted in destruction of organs like the pancreas, or permanent damage to nerves, as in MS, those patients would not end up in this diagnostic category.
You may, (or may not,) like my blog post on the state of the art w.r.t. actual immune function, as opposed to a stamp collection of facts about human immune systems. We have a wide range of interventions like antibiotics that manipulate immune response, but, when all is said and done, it is up to the patient's immune system to recover after treatment. (This is especially true in those cases where the intervention was based on mistaken assumptions, like antibiotics used to treat viral infections.) Most of the time we have no way to tell how well an immune system is working before it actually fails.
Many antidepressants have powerful effects on, e.g. enteroviruses. I can't think of one that doesn't have some effect on immune response. We could be treating infections by pathogens that don't qualify as acute infections, or we could be treating a dysfunctional immune response. At this point I can't say which possibility is correct.
My most recent hypothesis is that the recent discovery that healthy B-cells release a specific peptide which signals to other immune cells to limit recruitment of cytotoxic T-cells to inflamed tissues reveals a mechanism for limiting damage by T-cell invasion which may be defective after some infectious diseases. This looks like an example of quorum sensing by immune cells, something which I have expected to find, since there are plenty of examples of pathogens using quorum sensing to advance their own interests. I did not believe immune defenses were less sophisticated than strategies used by pathogens.
Patients who substantially recover after B-cell depletion by rituximab may be giving us a clue that some of the depleted cells were defective, but replacement cells from bone marrow were not. We still have not identified either which subset of B-cells were defective, nor what their defect may be.
Lymphocyte infiltration of salivary glands is fairly common, even in people without ME/CFS. There are many possible causes, like infection by CMV, and the type of lymphocyte gives a clue as to what those cells "think" they are attacking. Endothelial dysfunction also takes place in many cases labeled ME/CFS, and even T-cell infiltration of endocrine organs and some nerve ganglia. If this resulted in destruction of organs like the pancreas, or permanent damage to nerves, as in MS, those patients would not end up in this diagnostic category.
You may, (or may not,) like my blog post on the state of the art w.r.t. actual immune function, as opposed to a stamp collection of facts about human immune systems. We have a wide range of interventions like antibiotics that manipulate immune response, but, when all is said and done, it is up to the patient's immune system to recover after treatment. (This is especially true in those cases where the intervention was based on mistaken assumptions, like antibiotics used to treat viral infections.) Most of the time we have no way to tell how well an immune system is working before it actually fails.
Many antidepressants have powerful effects on, e.g. enteroviruses. I can't think of one that doesn't have some effect on immune response. We could be treating infections by pathogens that don't qualify as acute infections, or we could be treating a dysfunctional immune response. At this point I can't say which possibility is correct.
My most recent hypothesis is that the recent discovery that healthy B-cells release a specific peptide which signals to other immune cells to limit recruitment of cytotoxic T-cells to inflamed tissues reveals a mechanism for limiting damage by T-cell invasion which may be defective after some infectious diseases. This looks like an example of quorum sensing by immune cells, something which I have expected to find, since there are plenty of examples of pathogens using quorum sensing to advance their own interests. I did not believe immune defenses were less sophisticated than strategies used by pathogens.
Patients who substantially recover after B-cell depletion by rituximab may be giving us a clue that some of the depleted cells were defective, but replacement cells from bone marrow were not. We still have not identified either which subset of B-cells were defective, nor what their defect may be.