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Immunology in five-minute bites: T cells, cytokines and MHC

Discussion in 'General ME/CFS News' started by Simon, Nov 1, 2014.

  1. Simon

    Simon

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    Would you like to learn more about immunology, but not too much more? If so, then you might find this thread helpful.

    Immunology is probably the hottest subject in ME/CFS, but it's a spectacularly complex area that is made harder to understand by immunology's flair for impenetrable jargon and endless acronyms.

    I'm taking an 8-week online "Fundamentals of Immunology" course and thought I'd try to bring the highlights from the lectures to a wider audience. So I'll be posting relatively short pieces - that can be read in about five minutes - summarising what I think I've learnt.

    The course itself is free if you want to try it (you might want to check out Part 1 of the course too).

    Please watch the thread if you want to get updates, as I will only be posting from time to time
     
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  2. Simon

    Simon

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    Week one: MHC molecules aka HLA - which may have a role in ME/CFS

    MHC molecules are a good example of confusing immunology jargon and acronyms. They play a critical role in detecting pathogens and keeping us healthy, but the name "Major Histocompatibility Complex", MHC, doesn't give any clues. Histocompatibility refers to tissue matching, which is critical if you need an organ transplant. If the donor's MHC genes don't match yours then your body will reject the transplant, which is crucial. Yet the main role of MHC is nothing to do with transplants.

    Oh, and MHC is mostly used for mice and other animals, the same genes/proteins in humans are called HLA, short for "Human Leucocyte Antigen" (don't ask).

    MHC/HLA in ME/CFS and disease

    Ron Davis at Stanford believes that they type of HLA genes you have may influence the risk of getting ME/CFS, and certainly HLA gene variants have been linked to numerous diseases. One particular version of an HLA gene increases the risk of narcolepsy by 130 times. A version of another HLA gene conveys some protection against HIV developing into AIDS - though the same gene variant increases the risk of the autoimmune disease Ankylosing spondylitis. In fact, HLA genes are linked to a number of autoimmune diseases.

    MHC molecules help activate T-cells

    T cells are an important part of the immune system. Our lecturer refers to T helper cells as 'generals' of the immune system, co-ordinating the immune system response. T helper cells play a critical role in firing up antibody-producing B-cells, for instance. Cytotoxic T cells are more like infantry acting independently and killing off rogue cells such as those infected with virus.

    But T cells need to be activated first before they get going, and they are activated in part by antigens, which are helpfully defined as anything that the immune system recognises as foreign!), but we are talking here mostly about peptides, short pieces of protein. And antigens are what MHC molecules are about: they sit on the cell surface and hold out antigen morsels to the T cells. If the T-cell 'recognises' the antigen - in much the same way as an antibody recognises a specific antigen - then that will trigger activation of the T cell. In the case of cytotoxic T cells, that's curtain for the cell doing the presenting – the cell has just signed its own death warrant, but that’s the whole idea. Since cytotoxic T cells generally only recognise foreign antigen, and if the cell is displaying this it’s because it’s been infected, usually by a virus. By taking out the infected cell the cytotoxic cells are helping to contain an infection and protect other, healthy, cells.


    ’Don't kill me’: MHC I and Cytotoxic T cells

    Almost every cell in the body displays MHC I molecules, the imaginative name for the first of two types of MHC molecule. (Red blood cells and sperm don't display MHC I, but just about everything else does). The MHC I acts as a kind of Identity card, the way a cell proves that it is healthy and should be left in peace by marauding cytotoxic T cells that will kill any cell that doesn't pass muster. You could see cytotoxic T cells as an internal security force that's licensed to kill.

    The whole system is pretty elegant and very hard to cheat as the MHC I molecules pick up bits of whatever proteins the cell is producing. So if the cell is infected eg by a virus it will be manufacturing lots of viral proteins, and bits of these foreign proteins end up displayed on the MHC I molecules. That's curtains for the infected cell: once a cytotoxic T cell recognises that viral antigen it sends a signal to the infected cell to self-destruct.

    Some viruses try to evade this detection system by reducing the amount of MHC I molecules that get displayed on the cell surface. We have evolved a counter-measure to this: Natural Killer cells will kill cells that aren't showing enough MHC I molecules, just to be on the safe side.

    So that's MHC I: cell-surface molecules that act as Identity cards by displaying to cytotoxic T cells bits of whatever proteins the cell is making. It's a way for healthy cells to show to lethal cytotoxic T-cells that they are 'clean', while infected cells mark themselves for destruction. Cytotoxic T cells can also detect other types of damaged cells, including those that have become cancerous.



    MHC II: displaying enemy heads on pikes

    MHC II also display antigens, but while MHC I is on all cells, MHC II is used by the 'professionals'. That's professional immune system 'antigen presenting cells', such as macrophages, dendritic cells and B-cells. Their role is to pick up foreign antigen and present it to T helper cells to kick start the adaptive immune response. (Adaptive immune responses are very specific eg antibodies that recognise a particular viral protein, as opposed to ‘innate’ responses that recognises classes of pathogens eg recognising viral RNA, or bacterial cells walls.

    T helper cells don't act directly against an infection, but regulate other immune cells, especially the cytotoxic T cells we've just discussed and antibody-producing B-cells.

    The big difference between MHC II and MHC I is that MHC II presents foreign antigen, picked up from outside the cell, whereas MHC I presents self-antigen from inside a cell.

    Think of MHC II molecules as pikes used to display the heads of enemy pathogens to T helper cells. T cells can't recognise antigens on their own, but can when they are processed right and displayed on MHC molecules. Fussy, you could say.

    Bonus info! T helper cells, CD4 and HIV

    T helper cells carry the CD4 cell surface marker, which helps the cells lock on to MHC II molecules. You may have heard about CD4 counts as a way of measuring the status of HIV patients. Unfortunately HIV infects and kills T helper cells, reducing the ability of the body to target HIV itself. As (or if) the disease develops, the number of T helper cells falls, which is measured by the CD4 count in blood: a lower CD4 count means fewer T helper cells and is a sign the disease is progressing towards Aids.



    MHC molecules and organ transplant

    Having just said that T cells can’t recognise antigen on there is one unfortunate exception: some T cells will recognise foreign MHC molecules, though it’s not really clear why they do this. The result is that your body will ‘reject’ organs donated from someone else as cytotoxic T cells and T helper cells will attack the foreign tissue. However, if the donor has the same MHC molecules as you, the T cells won’t see any difference and the transplant should be accepted. There are hundreds (at least) of different types of MHC molecules so most unrelated people won’t be a match. However there is a one in four chance that your brothers and sisters will be a match, which is why searching for a donor usually starts with siblings (though even a sibling is unlikely to donate a heart….).
     
    Last edited: Jan 28, 2015
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  3. Lynne B

    Lynne B Senior Member

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    Thanks, Simon,

    This is a really interesting way to explain aspects of the immune system.

    I imagine you're finding the course fascinating. Hope you keep posting. I'm going to use this to look at my blood studies. I've never had any explanation for the results. In particular, what does it mean if you have high gamma globulin and low beta globulin? Hope you come upon an explanation of results like these sometime.

    Cheers, Lynne
     
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  4. Simon

    Simon

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    Thanks, Lynne
    The course is fascinating, though rather more detail than I'd like (only a fraction of which made it to the piece).

    I should stress I'm only looking at the theory/biology, and interpreting test results is way, way beyond me. Gamma globulins are the main class of antibodies. Beta globulins are not antibodies at all, a mixture of stuff that includes the complement proteins. This link might help a bit, but really, I'm out of my depth here:
    Globulins | Doctor | Patient.co.uk
     
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  5. Simon

    Simon

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    Making the antigens to display to T cells

    A short post (with videos! it's fun!) about how antigens are processed before they get stuck on MHC molecules. This might seem like too much detail, but remember that antigens are what activate T cells to launch their immune response. No antigens, no T cell response. No B cell antibody response either, as activated T helper cells are essential for B cells to mature into effective antibody-producing factories. Antigen processing matters.

    “Don’t kill me”: making antigens that show the cell is doing no harm

    Proteins don’t live forever and one estimate gives them an average half-life of just seven hours. They become oxidised by free-radicals or damaged in other ways and get recycled. These recycled proteins are the source of the antigens that MHC I display on the cell surface, to give cytotoxic T cells a window into what’s happening inside the cell.

    Mostly the antigens displayed on MHC I will be self-antigens, bits of normal proteins, and cytotoxic T cells don’t recognise self-antigens and they will leave the displaying cell in peace.

    But if there are rogue proteins in the cell, such as viral proteins resulting from a viral infection, cytotoxic T cells will recognise the viral antigen and force the infected cell to self-destruct - helping to contain the infection.

    The process of recycling proteins and generating antigens is pretty neat. First, a molecule called ubiquitin marks the damaged protein for destruction (ubiquitin as in “You Be Quitting”? Molecular names don’t have to be impenetrable). Ubiquitin-tagged proteins then head to their doom in proteasomes, cool molecular machines that shred used protein into small pieces for recycling.

    Watch the proteasome shred a ubiquitin-tagged protein [jump to 46 seconds: approx. 15 second sequence cued up and ready to go]



    Bits of shredded protein the right size get picked up and loaded onto MHC molecules, which then head for the cell membrane to display the antigen to patrolling cytotoxic T cells.

    Making the foreign antigen 'heads' to go on pikes for display to T helper cells

    While MHC I display antigens generated within the cell, MHC II displays bits of foreign antigen on that originate outside the cell. For example, macrophages engulf viruses, chew them up into small pieces of antigen (enemy heads) and stick them onto MHC II molecules (the pikes). These heads on pikes fire up specific T helper cells that happen to recognise that viral antigen, and the activated T helper cells launch a cascade of anti-viral activity.

    Sadly there’s nothing as flashy as a proteasome to process foreign antigen. In the first step, foreign matter (bacteria, viruses etc, or bits of them) is swallowed up by phagocytosis, a process also called endocytosis as shown here:


    The result is a capsule, or phagosome, inside the cell that contains the foreign matter, which is then digested by enzymes into small pieces of antigen.

    A second capsule containing empty MHC II molecules then fuses together with the antigen capsule, and antigen sticks on to the MHC II molecules, which then head to their surface: pikes bearing enemy heads to attract the attention of T helper cells.

    T cell antigens different to B cell antigens

    B cells often produce antibodies that bind to complete proteins, like viral coat proteins. It's a 3-D fit, like a key in a lock or a hand in a glove. By contrast, the antigens proffered by MHC molecules by T cells are short strings of amino acids that have no 3-D structure.

    MHC and disease: the antigen-binding site is key
    As I mentioned in the last post, mutations in MHC molecules are associated with numerous diseases including narcolepsy, and may yet prove to have a role in ME/CFS (according to Ron Davis at Stanford who wants to study human MHC genes [called HLA genes]). It turns out that most of these mutations affect the antigen-biding site of the MHC proteins, presumably stopping antigens binding properly to the MHC molecule. So the slightly tedious molecular detail of antigens and MHC molecules may be an important factor in understanding our own health.
     
    Last edited: Nov 10, 2014
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  6. MeSci

    MeSci ME/CFS since 1995; activity level 6?

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    I don't think this is always the case, is it? Immunoglobulins/antibodies are proteins, and some of them live for quite a long time.
     
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  7. Simon

    Simon

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    Sorry, that should have been average half-life - there is indeed a huge range (now corrected). I think secreted antibodies have a particularly long life
     
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  8. Simon

    Simon

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    How do T cells manage to recognise just about any foreign antigen?

    Just like antibodies, T cells can recognise just about any foreign antigen (including not just antigens out there already, but those yet to evolve too), and its this antigen recognition that activates they system. But how do they recognise so many different antigens?

    T-cell.jpg
    a particularly cute T cell

    T cells recognise antigens with their T cell receptors which are related to antibodies but as receptors they are attached to the cell membrane. And it turns out that T cell receptors can recognise just about any antigen for the same reason that antibodies can: both result from the extraordinary way that their genes are re-created as T and B cells develop and mature.

    T cells are born in the bone marrow. Stem cells there produce a steady stream on new, immature T cells that move directly to the Thymus, a small organ that sits below your throat.

    The Thymus is where T cells develop their ability to recognise antigens by recreating their receptor genes; the ‘T’ of T cells comes from Thymus. (By contrast, antibody-making B cells do most of their development in the Bone marrow.)

    T-cells-in-Thymus.jpg

    Normally the genes we inherit from our parents are the ones we use, simple as that. But in an extraordinary process, T cells (and B cells) re-create certain immune genes once they start to develop from stem cells. For T cell receptor genes, what we inherit from our parents is a gene-generating kit for making endless different T cell receptors genes, rather than a proper gene itself.

    Once T cells reach the Thymus they begin to create their very own, unique T cell receptor genes from this gene-generating kit. It's a complex process but the short version goes like this: Each original 'gene' has many, many regions, and the cell combines just three of these to create a new gene that is one of thousands of different possible combinations, each with the potential to bind a different antigen.

    Bit more detail: The cell selects one V (variable) region of many, one D (diversity) of many, and one J (joining) region of many to give a random new VDJ gene - check out this video (actually about antibody genes) which illustrates the principle - you only need watch the first thirty seconds.]



    Why not just have a lot of genes and save all this complicated faffing about?
    OK, so this is an extraordinarily complicated process to understand, takes a lot of time and involves a lot of energy and waste. Why not just have more genes ready to go? Two reasons:
    1. Not enough space: according to the latest evidence, we have around 19,000 genes. Carrying another zillion (even, conservatively, a billion) genes wouldn't be viable.
    2. We need to be ready not just for what's out there, but what's to come. Bugs evolve, fast. Bacteria can reproduce every 20 minutes. We take 20 years. So even if we had genes encoding T cell receptors against every pathogen going, they'd get out of date as bugs evolved and outpaced us. Instead, trying to cover just about everything gives us a better shot against evolving bugs.
    But T cells have another trick to create yet more variation in the genes and so the ability to bind even more different antigens. When the three regions get spliced together, special enzymes insert random nucleotides (the four bases, A, T, G and C that make up the coding part of DNA) between the regions changing the gene again. So even where two T cells have exactly the same VDJ combination in their receptor genes, the genes will be different because of these random additions. The result is vast numbers of different genes.

    A T cell receptor actually has two subunits called alpha and beta that work together as a pair to recognise antigen. The gene for each subunit re-arranges separately, with the beta gene going first. Each T cell with a successful rearrangement of its beta subunit expands into a clone of identical new cells. And each of those new cells then rearranges the alpha gene. So for every new, unique beta subunit there will be countless different alpha subunits.

    The combination of many unique alphas for every unique beta chains further increases the number of different possible T cell receptors, each recognising a different antigen.

    The end result of all this rearrangement of both alpha and beta chains is zillions of different T cell receptors that recognise zillions of different antigens.

    Unfortunately, many of these random permutations are complete duds - inserting random bases into a coding sequence usually wreaks havoc - and where that happens the cell dies. But zillions of T cells with properly assembled T cell receptors remain.

    There is one small problem to tackle: because these T cells now recognise zillions of different antigens, covering just about everything, they will also recognise just about every protein in healthy human cells. This is recipe for autoimmune diseases in abundance, and the next critical step is selection of those T cells that will actually work properly without destroying our own healthy cells.
     
    Last edited: Nov 10, 2014
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  9. MeSci

    MeSci ME/CFS since 1995; activity level 6?

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    Bet that took you longer than 5 minutes to write, @Simon! (It certainly took me longer than 5 minutes to read - and my foggy brain still couldn't absorb it all - I even forgot where the brackets were on the keyboard just then!).

    2 questions - apologies if the first one is already explained:

    1. What constitutes a "successful rearrangement of its beta subunit"?
    2. How many noughts are there in a zillion? :D
     
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  10. Simon

    Simon

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    Ah, sorry about the confusion, and thanks for the feedback. Will try to simplify next time out.
    A zillion? As many noughts as you like :), one estimate is 10 to the power of 15.

    ps and yes, did take me a little over the five minutes....

    edit:
    The new beta chain actually binds to a dummy alpha chain (an alpha lookalike) to make a 'pre-T cell receptor'. If that T cell receptor comes together and fits into the membrane (and probably some other tests too) then it counts as successful and the cell moves on to rearranging the alpha gene.
     
    Last edited: Nov 10, 2014
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  11. MeSci

    MeSci ME/CFS since 1995; activity level 6?

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    Confusion wasn't your fault. My brain was/is the problem. Another day I might be able to absorb it!
     
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  12. Simon

    Simon

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    You comment was really helpful. I just reread it and see what you mean. The problem is the material we are studying is phenomenally complicated (or 'just the basic details' according to the lecturers) and it's a challenge to simplify to a useful level for a wider audience.

    btw, now answered the other question you asked, in my previous post
     
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  13. Simon

    Simon

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    Why do we need to recognise every antigen out there?

    There are good reasons we go to all this trouble to make T cells (and antibodies) that can recognise just about anything:

    In the beginning there was only one form of immune system: the innate or natural system. This recognises generic threats such as ‘virus’ or ‘bacteria’ or ‘fungi’. It’s ready to go the moment the threat appears. Here’s the lecturer on my course, Dr Alma Novotny, demonstrating the the kind of generic recognition used by the innate immune system: if we saw someone dressed like this, we wouldn’t know anything about them, other than they were a threat. That's how the innate immune system works.
    [​IMG]

    Then, about 500 million years ago, came fish and with them came the first adaptive immune system. This add-on is more like a smart bomb, homing in on particular targets which for humans includes Influenza A virus, the bacteria that cause TB, and tapeworms. It adapts to whatever specific threat we face.

    The big advantages of this targeted approach are less collateral damage, greater effectiveness against the specific target – and less waste of resources: immune systems chew through a lot of energy.

    The drawback is that it has to be able to identify pretty-much anything, very specifically, rather than relying on recognising a general pattern. That’s why we have to go to so much trouble recognising zillions of antigens. Oh, and the adaptive immune system is slow: it can take 7-10 days to mount a really good response to a new infection. While that’s happening we continue to rely on the innate immune system to keep us alive by stopping the infection running rampantly out of control, even if it can’t stop it altogether.
     
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  14. Simon

    Simon

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    I realise I’ve lost a lot of people with my attempted explanations and will try here one more time to make things a little more comprehensible in this new post. If that doesn’t work, I’ll call it a day.


    T cell selection: Massacre of the wannabes

    So far the developing T cells have rearranged their T cell receptors in the Thymus so that between them they can potentially recognise zillions of different antigens. But they are not there yet – and most will be killed off: the selection of T cell hopefuls is a lot more ruthless than anything you see on X-factor.

    Positive selection

    Remember that T cells can only recognise antigen presented on MHC molecules (see post #2) so it's essential that T cells can bind to those molecules. If they don’t, they die.

    The Goldilocks principle

    [​IMG]

    Unfortunately for many developing T cells, binding to MHC molecules is not enough. They must bind it, but not too tightly. Not too much, not too little, but just right – which is known as the Goldilocks principle. There’s a really good reason for this approach. The whole idea is that T cells recognise specific antigens held on MHC molecules – that’s when you want them to bind tightly. If they bind tightly to MHC regardless of the antigen the result would be autoimmunity - any old MHC molecule would fire up T cells whether it was carrying self-antigen or a foreign one . So T cells that bind MHC too tightly must die too. It’s tough being a wannabe T cell.

    This first step is called positive selection as it positively selects T cells that bind MHC molecules just right. Most T cells never make it beyond this stage.

    this isn't relevant, but:

    [​IMG]

    Negative selection

    As you've probably worked out, the random creation of genes (post #8) will generate T cells that bind just about everything, which will include just about everything you are likely to find on or in healthy human cells. So the next stage, central to avoiding autoimmune disease, is removing all the T cells that bind to self-antigen. This step is really neat.

    A giant buffet of human proteins

    T cell development takes place in the Thymus and of course Thymus cells don't normally express, say, liver or kidney proteins. So how to remove T cells that attack these liver, kidney etcetera proteins before they head out into the body? Step forward a group of special cells in the thymus that are programmed to express just about every protein in the human body: liver proteins, kidney proteins, immune cell proteins, whatever – over 19,000 of them according to a recent estimate. It’s a bit like a giant buffet of human proteins, though a lethal one as any T cells that bind these human proteins will die. Well, that’s the theme of this section really, wiping out any T cells that won’t help - and T cells that recognise your own proteins would set off autoimmune disease.

    The upshot of all this T cell development in the Thymus is that:
    • First, T cells generate T cell receptors that can recognise almost any antigen (without needing a zillion different genes) and
    • second, ruthless selection ensures that only T cells that bind to MHC molecules and foreign antigen - but not self-antigen - are allowed to proceed.
    One way or another almost all new-born T cells that enter the Thymus from the bone marrow will die, but those that survive will provide us with critical immune protection against pathogens, parasites and even cancers.
     
    Last edited: Nov 12, 2014
  15. MeSci

    MeSci ME/CFS since 1995; activity level 6?

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    @Simon, I am getting a lot from your postings, and I am sure many others are too! It's just our ME brains struggling as usual to take in, retain and work with info, in your posts and others (including mine).

    The funny cartoons provide some welcome light relief too.

    I expect @Jonathan Edwards has already covered this, and I may even have replied - but...well, you know how it is.

    Do the
    have a specific name?

    I am very interested in the autoimmune hypothesis of ME and other illnesses, and I have gathered from Prof Edwards that autoimmunity is more likely to arise from the failure to delete autoimmune cells, rather than the generation of them, so I devour all info I can find relating to this, such as your posts in this thread. Although Prof Edwards reckons (and has probably explained why but I have forgotten :bang-head:) that it is B cells rather than T cells involved in ME.

    But until we know, we must consider all credible theories, I think - and maybe different autoimmune cells are involved in different subgroups.
     
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  16. Bob

    Bob

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    I'm enjoying your immune lessons too, Simon. :thumbsup:
    As @MeSci says, it nicely complements what Jonathan Edwards has been teaching us.
    Your text isn't difficult to follow - but it is a complex subject to grasp - and you're doing a great job of presenting it in bite-size chunks - I don't think you could make it any simpler without making it too shallow.
    So, keep the lessons coming please, if you're happy to :)
     
    Last edited: Nov 12, 2014
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  17. Simon

    Simon

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    Thymic epithelial cells
    Yes, same principle but I suspect the mechanism is different. Most B cell selection takes place in the Bone marrow, I believe. There is also peripheral selection, for T cells at least, that catches at least some of any self-reacting T cells that escape the massacre in the Thymus.

    And glad you find the posts helpful. You;re right though, it's very complex material. I'm hoping that at the end of my course I'll be able to understand Jonathan Edwards' posts.

    Thanks, Bob, glad you like them - just hit the like button on my posts: it really helps me to know what people find worthwhile, and what they don't.
     
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  18. Bob

    Bob

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    BTW, in case helpful for anyone, Jen Brea has recommended the following website, for learning about immunity...
    She says it's a "really basic, easy to understand immunology primer"... But I haven't looked at it yet:
    http://bitesized.immunology.org/
     
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  19. SDSue

    SDSue Southeast

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    @Simon Thanks so much for all the work you do getting information to PR members.

    I wonder if you could point me to the part of the course, or your writings, that covers cytokines.

    I have found a local osteopath who is having success with targeted treatment via cytokine nasal sprays. As you are likely aware, cytokines are currently being tested for use as adjuvants in nasal spray vaccines because of their profound affect on the immune system, and I could sure use a profound effect on my immune system! Because of all this, I'm very interested in learning more and possibly seeing this doctor.

    Thanks again for all your work.
     
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  20. MeSci

    MeSci ME/CFS since 1995; activity level 6?

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    I wasn't Simon last time I looked :lol: but maybe this thread would help.

    I don't think I've heard of cytokines being used therapeutically.
     
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