30. Immunology 1 - Diversity, Specificity, & B cells
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- เผยแพร่เมื่อ 11 พ.ค. 2020
- MIT 7.016 Introductory Biology, Fall 2018
Instructor: Adam Martin
View the complete course: ocw.mit.edu/7-016F18
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Professor Martin introduces the topic of immunity, defined as resistance to disease based on prior exposure. Beginning with vaccines as an example, he gives an overview of the immune system, followed by its properties of specificity, diversity, and memory.
License: Creative Commons BY-NC-SA
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This is an excellent lecture and a great lecturer. For just one lecture he gave so lot of information. Incredible! Thanks!
you literally can't present the same content in a better way. Excellent lecture and excellent lecturer!
Thank you so much sir and congratulation as well.
You have marked your footmark in the history.
Students even after a century will learn from your classes.
Cardi B farts and hundreds of million views, but this FREE gem of information has 30k views. The world we live in....
Excellent lecture. Very clear. Thank you.
Very helpful and inspiring, thank you.
Very clear and well -organized
Comprehensive and excellent presentation.
Very clear, and well-organized.
Well done Rodney for getting away from Del Boy.
I love your lecture just magical
Lc should be below hc for abs
The great lecture
Thank you sir ❤
Excelente
Thank you, professor ❤️
Hello
From where
41:45 HOW would a recombined allele suppress the recombination on the other allele? If it is not known yet with certainty, better not state it with certainty.
Great!!!!
To the memory aspect of it, does the time lapse between the 1st and 2nd response a factor into the efficacy of the secondary response, and the tertiary, and so on?? i.e. if you're exposed to the same antigen within days/weeks/months, vs. years vs. decades is the secondary response always as efficacious?
It depends on several things but two of them are the amount of Immune response that was generated 1st time and 2nd is how much mutation does that pathogen usually undergo?
If the memory system is generated (1), it will be reactivated everytime body encounters that pathogen unless it has changed its antigenic determinants so much from previous exposure (2) that the previous memory cell/Ab can no longer recognize it.
Beside that, probably response intensity decreases over very long period because "memory doesn't last forever".
Are they lectures on pharmacology .?
Best!
Is it possible to cancer treatment kill memory B cells? Like, our adaptive response will get damaged and our vaccines may turn ineffective...
Very interest ing
I have a question. In the example of herceptin, why not we just use the antibody totally generated from human (including the CDR), but instead, using the engineering to combine mouse CDR region with human to do immunotherapy? Thanks.
Ethics. Also you need to have a human with breast cancer willing to give you their antibodies. Or their B cells matured against the cancer. And you need a healthy human who'd let you inject them with the breast cancer cells. It's called hybridoma tech from which Herceptin MAb is generated. Look it up.
Antigen does not always activates the immune system buh immunogen does
I am super excited about the combination of the facts that AlphaFold has solved protein folding problem and there exists antibody therapy. Bring it on antibiotic resistant drugs!
Excellent lecture & Thank you!!!
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Is it for microbiology?
great professor. I am just not clear of the gene rearranging in B cell diversity. can anyone make it simpler?
Basically DNA segments are being "cut" by RAG enzymes to end up with the final variable part of the Ig. Heavy chains are made of a V segment + D segment + J segment ( there are different V and D and J segments in our genome which is part of the reason why Igs have a high polymorphism ). First the D and J segments get together by "cutting" what's between them, then the V and DJ segments get together. After splicing the constant region of the chain is assembled with the VDJ. for the light chain, gene rearranging happens after proliferation and there's only a V and a J segment so you end up with a VJ variable section. V stands for variable, D for diversity and J for junction if I remember correctly. RAG enzymes are only active in T and B cells (sorry if there are mistakes I'm French and only a 3rd year biology student lol)
Each early (not mature) B cells have same antibody gene locus. when a UNKNOWN antigen enters to the body, T cells release cytokins and starts the proliferation of B cells but when B cells proliferate, each B cells goes a type of mutation. first mutation is VDJ rearrangement. this process shortens the VDC gene locus that is very long in unmature B cell. İn each locus (V, D or J but not in C) one gene is chosen and other genes are cut forever. This makes all B cells to produce different antibodies. At this time this antibodies are not secreted. It is only on cell surface and it is IgM type. Combination of three genes produce a high number of anibody diversity. But some antibodies are not suitable because some antibodies are for human tissue and cell antigens. So T cells recognizes it whith MHCII and orders to the B cells to kill himself (this means apopitosis). After this APC (antigen presenting cells) dendritic cells tests the antigens on B cell's surface that is it appropriate for the antigen that entered to the body. If the B cell can attach to the dentritic cells with its antibody , it will be chosen. The other B cells that can not attach to the antigen on dentritic cells' surface, they won't survive and they will die.
In a siple way for explanation: Fishes produces millions of eggs to have a baby fish. all eggs can not survive. All eggs go to selection process and the most attractive, strong, healhy egg will survive and other will die. To get a strong and right selection nature uses probabilty. To get a good chance, it dice millions time.
Second step is antibody maturation and for this B cells goes to hypermutation in lymph nodes. This is more complex and this is real mutation that our body simulates to be done. After this hypermutation, antibody that is produced by selected (chosen) B cells has mpre affinity and more selectivity. After first exposure to the antigen, second and more exposures makes this somatic hypermutations again and antibody becomes also more durable.
third step is Class switch: To secrete antibodies, B cells must change to plasma cells. but after VDJ rearrangement and somatic hypermutations, it can only produce IgM antibody (and some IgD). it is very big antibody and for a short time in infection, it is effective but it has disadvantage. it can't be secreted out of blood vessels. so to protect the intestines and respiratory sytems, antibody genes switch to IgA , IgE and IgG antibody type. this is called Class switch. Aafter class switch each B cells one type of Immunglobuline. IgA, G, M and with one type Light chain.
28:24 time stamp
B cell secretes? Sometimes..lots of guys recognized
T cell nmscretes..
Recognizes peptides....
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31:47
16:02
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Both T cell and B cell originate from bone marrow. Then B cells migrate to, but not produced by, the thymus.
You mean T cells.
, 😒
"The "B" comes from the bone"
I thought it came from the bursa
Bursa in relation to chicken which equivalents to bone marrow in mammals
Protein mediated....adaptive...antibodies...cell mediated.
B cells....one marrow...virus....
basophils?
Cell...tissues...mediated
Both adaptive.. antigens.
Father projections...psych..on males?
Same mother..?
Holistic health and education habits..
B cll scretes !! Has polypeptide chain...sticking out?
Antigen on virus bind.?
T cell..a b
The thundering lunch biochemically plug because knowledge extracellularly practise during a ambiguous ex-husband. dramatic, mixed club
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