A Basic Guide to Immunology


Right guys, I’ll try (being non-medic) and give you a very basic insight into immunological mechanisms. …Sit up straight at the back!!, and stop munching on that bar of chocolate – swallow it now!! (shouts he wearing his demon headmaster wig) - LOL

You will know doubt be familiar with allergic reactions involving IgE antibodies. For example, someone who suffers from asthma due to dust mites will suffer from what is described as an immediate Type 1 allergic reaction, sometimes also called antibody-mediated reactions because it involves the production of IgE antibodies which in turn produce inflammatory chemicals like histamine, etc.

Now there are some important immunological details (“the dark side” as I sometimes call it) that are not openly communicated by GPs and are often excluded from general asthma/allergy books. Probably this is to avoid confusion due to the subject complexity.


Immune function (immunity) is split into two separate but overlapping components; Non-specific (innate) and specific immunity (adaptive). Although each of these host defences are described separately below, they are activated simultaneously and function synergistically to prevent and control infection. Host defences are regulated by T lymphocytes (T-cells) and this action is referred to as cell-mediated immunity. T-cells take their name from the Thymus gland, the point where T-cells are derived.

Non-specific immunity is the primary defence and non-specific component of the immune system such as the skin, mucous membrane and systemic defences. Non-specific immunity promotes inflammation as a defence mechanism. Generally speaking, it is only when the primary defence system has been breached that specific immunity will be signalled into action.

Specific immunity is the specific component of the immune system which initiates an immunological response when a person encounters a fungal pathogen, allergen, etc. As I said above, this does not become fully active until the non-specific defence system has been penetrated.

Specific immunity is provided by the release of antibodies (IgG, IgA, IgM, IgD & IgE) but let’s not go there just now. …Pay attention, please!! Antibodies are derived from B cells, also known as B lymphocytes. They take their name from the bone marrow, the point where B cells originate. B cell responses to most antigens are absolutely dependant upon T cell help.


If we look in more detail at T-cells (but still in a general sort of way), there are two main types of T-cells (there are others also). The first type are called T-helper cells (their text book name being CD4), and the second type are called T-suppressor cells (their text book name being CD8). Furthermore, T-helper cells can be broken down further into sub-populations. Does anybody know what these are called?, come on, quick, give me an answer? Much too slow. …You at the back, stop peering out of the window, you will not find the answer out there!! That is not a window of opportunity!!

Okay, now where was I, …yes, sub-populations – The helper cell sub-populations are normally referred to using their text book names Th1 & Th2. We will not talk about what Th1 and Th2 cells do (or for that matter Th0, Th3, Tr1) we will attempt to enlighten you another day when the temperature in here is a bit chillier to stop you falling asleep.

It is noteworthy that suppressor cells also have a sub-population and these are normally referred to using their text book names Tc1 & Tc2. But as I said above, let’s not go there today!


So going back to the T-cell, …why are T-cells so important? ..some mumbling from someone who hasn’t fallen asleep yet. Wake up you horrible lot!! Do you think I have nothing better to do than stand here sprouting forth with this medical claptrap!

T-cells are extremely important because they orchestrate and control ALL immunological functions. The T-cells work a wee bit like the engine management system in the modern car, by ensuring the correct level of immunological response is applied and withdrawn relative to the strength and potency of the invading allergen, bacteria, etc. The T-helper cells promote a vigorous immunological response (lets say by stimulating IgE production), and the T-suppressor cells hold back, slow down and taper-off the immunological response. The T-helper and T-suppressor cells work very closely together and it is this working relationship that is referred to as the T-helper/suppressor cell ratio (in text book terms CD4/CD8 ratio). In a healthy person the CD4/CD8 ratio is said to be 1:1 or even 2:1. If the ratio is changed in some way (either by an inherited characteristic or acquired) then this will affect the way in which the immunological response is applied/withdrawn. At one end of the immunological spectrum will be suppression of immune response leading to infection (possibly fungal respiratory infection) and at the other end will be hypersensitivity leading to autoimmune disease (possibly rheumatoid arthritis). And of course there is a whole range of immunological dysfunctions in between.


Well, do you know if an incorrect CD4/CD8 ration can be corrected? Come on guys, we are just about at the end of the topic for today so please show a wee bit more enthusiasm and stop slouching on your desk!

In principle it can be. This is called modulation or immunomodulation, where the ratio of CD4 to CD8 cells would artificially be adjusted/manipulated back to the nominal 2:1 ratio. The correct level of modulation is the difficult part because there are so many variables and corrections/counter-corrections going on in the body, plus this is very individual treatment and what may work well for one person may not have the desired effect on the next person.


So what treatments are available. Well guys I think the period bell is about to ring, so I will conclude this lecture by saying that treatments for T-cell modulation are very much experimental at the moment with consultants prescribing various types of immunosuppressive medicines like azathioprine, methotrexate and cyclosporin with varying degrees of success.

Cyclosporin appears to be the better option as it is a more selective immunosuppressant because its main site of action is the CD4 T helper cell population. From this, it would appear that azathioprine and methotrexate are not so selective and therefore will also suppress the T suppressor cell (CD8) population. The inference being that little (or no) modulation between CD4 and CD8 cells can be achieved using these other immunosuppressive meds. It is my opinion that immunosuppressants should not be prescribed if there is evidence that the immune system is already depressed.

Azithromycin is not an immunosuppressant but it does cause immune system modulation. Azithromycin is a macrolide antibiotic with immunomodulatory effects and this appears to be prescribed to asthmatics for its anti-inflammatory properties as well as its antibiotic properties. According to the literature, the modulatory mechanisms of azithromycin are effective but not clearly understood. It is my opinion that azithromycin should not be prescribed if there is evidence that the immune system is already depressed.

Sorry guys, but that’s it for today, and I hope you have been taking notes because I will be testing you on this next week – LOL.


5 Replies

  • Thanks Deek!

    have a wee dram!

    Will print it off for some bedtime reading over a neb!

    Love & wigs


  • Hi Derek,

    Some lighthearted 'observer' feedback now...


    As a former Ofsted/QCA and currently occasional English UK (formerly British Council) Inspector I would have to award a grade of Outstanding/point of excellence for your knowledge of the immune system and ability to transcribe that knowledge into – almost - non medical terminology.

    Opportunities for improvement.

    However, concerning the topical and much favoured ‘learner centred’ approach towards teaching the likes of us hoi polloi, a, satisfactory/ point met would be the recommended grade!

    Munching on chocolate? Small potatoes! Chocalate improves mood and subsequent concentration. Recommendations and further training include the focus upon an improvement in critical thinking skills via the use and practise of research activities. In short challenging learners' conventional thinking via the formidable power of KNOWLEDGE.

    Finding a teaching strategy that engages the whole audience or student body can be very difficult, the ‘holy grail’ of teaching if you like!

    Differentiated teaching activities are successful, as can be taking into account preferred learning styles. Some of us are visual learners, some auditory, some kinaesthetic, and some just plain off this planet!

    Using ‘real life’ scenarios as a vehicle for motivating ‘none engaged’ learners,- you know the ones that are distracted by ‘windows of opportunity’ - always merits a high grade!

    But all in all not a bad lesson! Lots of detail for discussion next week!

    Mia (wearing her Princess Leia observation wig)

    PS What was the homework?!

  • Dr Deek, I have a question. Can you tell me what the difference is between an anaphylactic reaction and an anaphylactoid reaction, except for the former involving IgE and the latter IgG?

    Much obliged.

    Wigs off to ya,


  • Hi Becky (…Dr Deek indeed, as he pulls wig forward to hide his blushes – LOL)

    Anaphylactoid Reactions …Mmmm, very interesting.

    Until you mentioned it Becky, I was not aware of the term anaphylactoid reactions. Although I am aware of haptenic reactions, which would appear to mean the same thing, just known by a different name.

    Haptenic reactions have been reported in connection with occupational exposure to certain low molecular weight chemicals known for their ability to cause occupational asthma WITHOUT previous exposure to prime the immune system, unlike antibody-mediated reactions where previous exposure is an absolute requirement. It is also recognised that haptens are so potent that they can cause asthma in persons with no previous history of asthma/allergy. Haptenic reactions are not specific to the occupational setting and many every day chemicals, substances and medication that people can come into contact with, are known for their ability to cause haptenic reactions.

    Haptens are capable of directly causing degranulation of mast cells with no evidence of IgE involvement. As an example, inflammatory chemicals like histamine (normally associated with IgE reactions) are released due to degranulation of mast cells. The normal IgE antibody-mediated mechanism is bypassed when a person is exposed to haptens and therefore no measurable difference in IgE will be noted.

    It is noteworthy that certain factors can elevate the risk of haptenic reactions. Beta-blocker medication and smoking are said to be adjuvants (vehicles for enhancing antigenicity).

    You mentioned the involvement of IgG in anaphylactoid reactions. This appears to be beyond my level of knowledge. Apparently anaphylactoid reactions can be cyclic with a second late phase reaction happening several hours after the initial reaction. The late phase part of the reaction could involve IgG antibodies as IgG reactions are described as Type 4 (delayed reactions). I would also point out that IgG reactions are common in food allergy, although this probably has no relevance to your query.

    I hope this helps a wee bit.


  • <Sticks hand up>

    Please Sir, this morning's Metro (that respected source of scientific knowledge) reported on a study which found chocolate boosts brain power. I feel we should be encouraged to eat/drink it during class!

    (My rusty A-level biolgy does need all the help it can get)