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A level biology difference between humoral and cell mediated immunity

Hello,

I am a little stuck on the difference between what humoral and cell mediated immunity is. My text book states:

"In humoral immunity the body responds to antigens found outside the cells (e.g bacteria, fungi and antigen presenting cells)"

But I thought that in the cell-mediated immunity this was also the case.

Does anyone have a good explanation to the difference between the two (I am doing OCR A level Biology)

Thanks!
Humoral immunity involves antigen recognition followed by conversion of B lymphocytes to plasma cells [rich in ER and mitochondria - work out why], and these synthesize antibodies [Y-shaped proteins each molecule of which is made of two light chains of polypeptides and two heavy chains [go to google images] - this antibody then neutralizes, conglomerates or precipitates the antigen thus deactivating the pathogen. [antibodies are divided into five main classes e.g. IgG [immunoglobulin G] is a small antibody molecule that is made in large amounts and can cross the placenta to protect the baby; IgM has 5 binding sites for antigen [large molecule] and is usually the first type generated by plasma cells.

Cell-mediated immunity involves exactly that: phagocytosis of the pathogenic organism by T lymphocytes, neutrophil leukocytes and macrophages. It is particularly important in viral infections, partly cos viruses are minute so easily engulfed. e.g. the AIDS virus attacks these T cells, and one of its main clinical features is fulminating viral infections e.g. toxoplasmosis; cytomegalovirus infection.

Hope this helps: also look up [esp for A* in synoptic Q] IgA in secretions; dendritic cells; antigen recognition cells; memory cells; killer T cells; helper T cells.

Hope this gets the ball rolling for you!
Be safe!
M
Reply 2
Original post by macpatgh-Sheldon
Humoral immunity involves antigen recognition followed by conversion of B lymphocytes to plasma cells [rich in ER and mitochondria - work out why], and these synthesize antibodies [Y-shaped proteins each molecule of which is made of two light chains of polypeptides and two heavy chains [go to google images] - this antibody then neutralizes, conglomerates or precipitates the antigen thus deactivating the pathogen. [antibodies are divided into five main classes e.g. IgG [immunoglobulin G] is a small antibody molecule that is made in large amounts and can cross the placenta to protect the baby; IgM has 5 binding sites for antigen [large molecule] and is usually the first type generated by plasma cells.

Cell-mediated immunity involves exactly that: phagocytosis of the pathogenic organism by T lymphocytes, neutrophil leukocytes and macrophages. It is particularly important in viral infections, partly cos viruses are minute so easily engulfed. e.g. the AIDS virus attacks these T cells, and one of its main clinical features is fulminating viral infections e.g. toxoplasmosis; cytomegalovirus infection.

Hope this helps: also look up [esp for A* in synoptic Q] IgA in secretions; dendritic cells; antigen recognition cells; memory cells; killer T cells; helper T cells.

Hope this gets the ball rolling for you!
Be safe!
M

Hello! Sorry for the very late reply. I was not expecting anyone to respond, thank you very much for that explanation! You have helped me a lot!



Thanks!
Original post by macpatgh-Sheldon
Humoral immunity involves antigen recognition followed by conversion of B lymphocytes to plasma cells [rich in ER and mitochondria - work out why], and these synthesize antibodies [Y-shaped proteins each molecule of which is made of two light chains of polypeptides and two heavy chains [go to google images] - this antibody then neutralizes, conglomerates or precipitates the antigen thus deactivating the pathogen. [antibodies are divided into five main classes e.g. IgG [immunoglobulin G] is a small antibody molecule that is made in large amounts and can cross the placenta to protect the baby; IgM has 5 binding sites for antigen [large molecule] and is usually the first type generated by plasma cells.

Cell-mediated immunity involves exactly that: phagocytosis of the pathogenic organism by T lymphocytes, neutrophil leukocytes and macrophages. It is particularly important in viral infections, partly cos viruses are minute so easily engulfed. e.g. the AIDS virus attacks these T cells, and one of its main clinical features is fulminating viral infections e.g. toxoplasmosis; cytomegalovirus infection.

Hope this helps: also look up [esp for A* in synoptic Q] IgA in secretions; dendritic cells; antigen recognition cells; memory cells; killer T cells; helper T cells.

Hope this gets the ball rolling for you!
Be safe!
M


Can you please describe briefly how T killer cells are activated? Does this require an interaction with an antigen presenting cell? If so since T killer cells bind to MHC-I what prevents them from destroying the antigen presenting cell in the process (how does a T killer cell distinguish a virally infected cell displaying viral antigens on MHC-I from a dendritic cell displaying viral antigens on the same molecule)? I have seen the B cell activation described clearly in textbooks but I'm yet to find a clear description for this. Thanks.
(edited 1 year ago)
Original post by macpatgh-Sheldon
Cell-mediated immunity involves exactly that: phagocytosis of the pathogenic organism by T lymphocytes, neutrophil leukocytes and macrophages.

Are T lymphocytes phagocytic?
Original post by thomas.rhett
Are T lymphocytes phagocytic?

Good morning Thomas (?) - are you also called Tom? {I ask cos in my uni hockey team [well one of them] there were a number of Toms - for some reason any Tom I come across plays hockey [great news oc cos hockey is THE game, fast, skilled and played by true ladies and gentlemen!] - do you play? :colondollar:

OK coming to the point, yes absolutely! They are one of the types of "soldiers" in our body that "eat" pathogens - they reside in the interstitial fluid [the transudate that is forced out of blood vessels by the hydrostatic pressure created by the heartbeat [oc minus the osmotic pressure in oppo direction]], so they act mainly in the extravascular [outside blood vessels] compartment, in common with macrophages [the equivalent of macrophages within the vasculature are the monocytes [you can identify a monocyte by its round nucleus that nearly fills the entire cell, yeah?].

Check out the pic on link below of a T lymphocyte {what organelle does it have plenty of? Why?] Try to work it out yourself; if stuck, do ask me again - I shall guide you.

https://www.google.co.uk/search?q=t+lymphocyte+electron+micrograph&hl=en&tbm=isch&sxsrf=APq-WBsLvOHXWrlpKDHuiIikfTwzr2cQSw%3A1649652638575&source=hp&biw=1348&bih=648&ei=nrNTYqeCIcn6gAawn4ugDw&iflsig=AHkkrS4AAAAAYlPBrkAM2fvBy8GK104A-n2NwdvXwemT&ved=0ahUKEwinyZf8mov3AhVJPcAKHbDPAvQQ4dUDCAc&uact=5&oq=t+lymphocyte+electron+micrograph&gs_lcp=CgNpbWcQAzoHCCMQ7wMQJzoLCAAQgAQQsQMQgwE6BQgAEIAEOggIABCABBCxAzoICAAQsQMQgwE6BggAEAgQHjoECAAQGFAAWKW6AWCtwwFoAHAAeACAAeYCiAH8EpIBCDI5LjIuMC4xmAEAoAEBqgELZ3dzLXdpei1pbWc&sclient=img#imgrc=sFSBDEin4lGarM

To answer your other Q [bit more involved] I need to supply fuel to my brain = sausage, egg & bacon [+ nice hot cuppa tea in this freezing British "spring"] lol! :colondollar:

Watch this space!
M
Original post by thomas.rhett
Can you please describe briefly how T killer cells are activated? Does this require an interaction with an antigen presenting cell? If so since T killer cells bind to MHC-I what prevents them from destroying the antigen presenting cell in the process (how does a T killer cell distinguish a virally infected cell displaying viral antigens on MHC-I from a dendritic cell displaying viral antigens on the same molecule)? I have seen the B cell activation described clearly in textbooks but I'm yet to find a clear description for this. Thanks.

@thomas.rhett

Hi there sorry about long delay - you must be thinking "how many sausages does this guy consume, man?"!!:colondollar:

One reason for the delay was that you posed a good Q so that I had to research this a bit. The info on this is highly complex, so I am not sure how to explain it to you in an easily assimilable way [I presume you are doing A levels?].

To put it simply, MHC molecules are not the sole medium that are recognized by the cytotoxic T cell or natural killer T cell. There is a series of other molecules [mostly proteins, but also some glycolipids, etc] that are present on the pathogen BUT NOT on the APC, which allow the T cell to distinguish between the two. [as it seems that you like to learn detail, I shall mention two diverse examples: a] CD cluster of glycoproteins, particularly CD8 in the case of killer cells; and b) low molecular weight phosphate-containing non-proteinaceous antigens present on a wide spectrum of bacteria.]

In addition, there are two main types of cytotoxic T cells [alpha-beta and gamma-delta], depending on the specific protein chains that they express; and there is s-t called a TCR [T cell receptor]; the latter aids the activation of cytotoxic T cells by APCs.

Apologies iof this sounds convoluted - can you help with your recent training @Jpw1097? - thanks!
Original post by macpatgh-Sheldon
@thomas.rhett

Hi there sorry about long delay - you must be thinking "how many sausages does this guy consume, man?"!!:colondollar:

One reason for the delay was that you posed a good Q so that I had to research this a bit. The info on this is highly complex, so I am not sure how to explain it to you in an easily assimilable way [I presume you are doing A levels?].

To put it simply, MHC molecules are not the sole medium that are recognized by the cytotoxic T cell or natural killer T cell. There is a series of other molecules [mostly proteins, but also some glycolipids, etc] that are present on the pathogen BUT NOT on the APC, which allow the T cell to distinguish between the two. [as it seems that you like to learn detail, I shall mention two diverse examples: a] CD cluster of glycoproteins, particularly CD8 in the case of killer cells; and b) low molecular weight phosphate-containing non-proteinaceous antigens present on a wide spectrum of bacteria.]

In addition, there are two main types of cytotoxic T cells [alpha-beta and gamma-delta], depending on the specific protein chains that they express; and there is s-t called a TCR [T cell receptor]; the latter aids the activation of cytotoxic T cells by APCs.

Apologies iof this sounds convoluted - can you help with your recent training @Jpw1097? - thanks!


Thanks for your reply and taking time to look into my question.

My question is not how T killer cells distinguish between pathogens and APC but between APC and a virally infected cell.

T killer cells AFAIK do not interact with pathogens directly. According to textbook, T killer cells are activated when they interact with an APC which results in clonal expansion. A naïve T killer cell binds to an APC using its TCR, if TCR is complementary to the antigen and this antigen is presented on MHC I on APC. Now virally infected cells also present antigens on MHC I and activated T killer cells bind to body cells presenting antigens on MHC I that are complementary to TCR and destroy those cells. What I don't understand is why activated T killer cells don't destroy APC that are not virally infected but also present the same antigen on MHC I in order to activate T killer cells, e.g. dendritic cells.

Thanks again and I know I definitely should not waste time on this but it does bother me. By the way, rumor has it that sausages are not good for coronary arteries!
Original post by thomas.rhett
Thanks for your reply and taking time to look into my question.

My question is not how T killer cells distinguish between pathogens and APC but between APC and a virally infected cell.

T killer cells AFAIK do not interact with pathogens directly. According to textbook, T killer cells are activated when they interact with an APC which results in clonal expansion. A naïve T killer cell binds to an APC using its TCR, if TCR is complementary to the antigen and this antigen is presented on MHC I on APC. Now virally infected cells also present antigens on MHC I and activated T killer cells bind to body cells presenting antigens on MHC I that are complementary to TCR and destroy those cells. What I don't understand is why activated T killer cells don't destroy APC that are not virally infected but also present the same antigen on MHC I in order to activate T killer cells, e.g. dendritic cells.

Thanks again and I know I definitely should not waste time on this but it does bother me. By the way, rumor has it that sausages are not good for coronary arteries!

As @macpatgh-Sheldon has said, it's because antigen presenting cells express other proteins such as CD80 and CD86 which bind to CD28 on T cells, causing T cell activation. Virally infected cells do not present CD80/CD86 It's not as simplistic as cytotoxic T cells kill all cells which present their cognate antigen with MHC I.

I think you're probably a bit like me, in the sense that you always have to understand why. As you've said though, it's definitely not worth wasting your time on small details like this, especially at your level. I have wasted so much of my time researching tiny details, but eventually you realise it's just not worth it.
Original post by Jpw1097
As you've said though, it's definitely not worth wasting your time on small details like this, especially at your level. I have wasted so much of my time researching tiny details, but eventually you realise it's just not worth it.

This is so true - particularly for topics like immunology, where you can keep peeling away the layers of a never-ending onion. Part of doing well in examinations like A level is being able to prioritise work and learning, and know when you're going over and above. There aren't enough hours in the day to read everything.
Original post by Jpw1097
As @macpatgh-Sheldon has said, it's because antigen presenting cells express other proteins such as CD80 and CD86 which bind to CD28 on T cells, causing T cell activation. Virally infected cells do not present CD80/CD86 It's not as simplistic as cytotoxic T cells kill all cells which present their cognate antigen with MHC I.

I think you're probably a bit like me, in the sense that you always have to understand why. As you've said though, it's definitely not worth wasting your time on small details like this, especially at your level. I have wasted so much of my time researching tiny details, but eventually you realise it's just not worth it.


Thanks a lot for clarifying the issue.

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