Humoral Immunity - Adaptive Immunity part 2, Animation
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- čas přidán 11. 06. 2024
- (USMLE topics) Steps of antibody mediated immunity, including affinity selection.
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Voice by: Ashley Fleming
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B-cells develop in the bone marrow and complete their maturation in the spleen. B-cells are formed in billions of variations, each carrying a unique surface protein, called B-cell receptor, BCR. Just like T-cells, they also learn to not react to the body’s own antigens; those that react to self-molecules are eliminated or ignored. The majority of mature B-cells - follicular B-cells, circulate to secondary lymphoid organs. T-cells and B-cells are usually separated into defined T-cell and B-cell zones within these organs.
Specific immunity relies on the invading pathogen finding a match among these many variations of B-cells. Only cells that can bind to the pathogen, can be activated to produce antibodies. B-cell surface receptors, BCRs, are actually membrane-bound antibodies.
An antibody is basically a protein whose structure consists of variable and constant regions. The variable regions give the antibody its uniqueness, much like the bit, or blade, of a key. This is where it binds to a specific antigen, which is the lock.
There are several classes of antibodies, differing in their constant regions. Different antibody classes engage different mechanisms to neutralize the antigen. The surface receptors on B-cells are IgM and IgD molecules.
Each B-cell has thousands of identical copies of BCR on its surface. When a pathogen binds, it usually binds to several of these receptors, linking them together, triggering endocytosis of the pathogen. B-cells then cut the pathogen into pieces and display them on MHC-II molecules on their surface. Thus, B-cells now become antigen-presenting cells, but are not yet activated. In most cases, activation of antigen-primed B-cells does not happen until they are stimulated by antigen-specific T-helper cells.
Nearby, in the T-cell zone, T-helper cells are activated by dendritic cells carrying antigens of the same pathogen, and become effector T-helper cells. Some of these effector cells leave lymph nodes for the site of infection, while other, namely the follicular helper cells, migrate to T-cell B-cell borders, and bind to the antigens presented by B-cells. This interaction triggers T-cells to produce helper factors, which activate B-cells.
Activated B-cells undergo first rounds of proliferation and differentiation, giving rise to the first batch of plasma cells producing antibodies, mainly of IgM class; and a group of cells that are committed to become memory B-cells. The latter undergo antibody class switching; and form a so-called germinal center, where they go through cycles of multiplication and hypermutation in the immunoglobulin gene. This process produces slightly different variations of the same antibody, which are then subject to a binding test to the same antigen. Those that no longer bind are discarded, while the remaining compete for binding to antigen-specific T-helper cells. B-cells with the highest affinity to the antigen win the interaction with T-helpers and exit the germinal center. They can either become long-lived memory B-cells, or differentiate into antibody-producing plasma cells. This second batch of plasma cells produces better antibodies and lives longer than the first batch. They also make antibodies of different classes (predominantly IgG), which neutralize the pathogen in many different ways.
Upon reexposure to the same pathogen, memory B-cells mount a much faster immune response.
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What an excellent diction, not too fast, so clear, just perfect! Graphics are great, too!
Clear to you perhaps, but only because you’ve studied the subject before. For a beginner who has only seen the prior videos in the playlist, this humoral immunity video after 2:22 is incredibly difficult to follow.
If i understand anything related to humoral immunity, it's because of this video
Spectacular way of explaining, highly recommend ❤❤
👌👌🙌👏👏 I would suggest students to watch this video after 1 reading of humoral immunity.
Hey
Such a useful and amazing channel!! Everytime I’m overwhelmed regarding my studies, this channel lifts me up and makes me more interested to learn than ❤❤
Excellent video
very helpful plz keep up. easiest way to refresh
Your Videos are extremely help ful ..
Thank you so much
Thank you
it clear to understand and perfectly explained..thanks and keep it up.
Very clear explanation, easy to understand. I'd like to suggest ( ask) that you make sometime a video to explain what is known abour how the excess of iron in erythrocytes due to hemochromatosis, damages macrophages that are recycling erythrocytes and may cause arthritis. Your work is great, thanks!
Brilliant! Thank you for these videos. I imagine many people like myself have become interested in the immune system because of the present Coronavirus pandemic. These presentations are about as clear as you can get!
perfect
Good stuff 👍🏽
Excellent video with good explanation.
مستغرب انو مشاهدات القناة هذي مرا منخفضة رغم الشرح الرهيب الي يقدموه
Ummmm what?
Your explanation is very nice 😜😜😜
Video on the immune system producing antibodies that attack other cells such as platelets (ITP) would be interesting.
My body does this! Hell yeah
Excellent 😭
Thanks 😅
So interesting 😅😊
Umoral imunity (Anticorps) can eliminate bacteria whitout involving celular imunity? If no, what happend when you have antiicorps and celular imunity system is low? Thanks.
Ngl I'm very confused but the video is great
How much manner a B cell or T cell can be activated ?
and what is the purpose of each different immunoglobulin ? and how in reality the immune response are regulated by Treg cell ?
and for finish ...
Why we need CD8 cell that recognize only a specific MHC-1 corrupted by a specific virus if we can directly recognize that the MHC-1 is corrupted ? and after that we kill the cell
Plz provide in hindi too.
Didn’t understand how class switching and infinity maturation took place until after seeing this super simplified video. It doesn’t get to the nitty gritty stuff but it still explains the pathophysiological process better than any 2 hour video that breaks down the cytokines and cellular interactions like Najeeb, and FA General Principles. One thing I’m still confused about is I realized a lot of materials get carried away with trying to explain that naive B cell activation could be as a result of direct interaction with naive T-helper or from IL-4 and IL-5 from another APC activated T-helper2 and that either B7-CD28 or CD40-CD40L interaction can be the co-stimulatory signal for T-helper2 activation as a result correct?
Example so any APC perhaps dendritic cells can use B7-CD28 interaction as a costimulatory signal for T cell activation from which it releases IL-4 and IL-5 for B cell activation OR B cells can use CD40-CD40L interaction as a costimulatory signal for when it acts as a APC and binds directly to the naive T-helper2 causing the activation of the cell and the subsequent release of IL-4 and IL-5 for the activation of the APC B cell. And macrophages also contain both B7 and CD40 however the CD40-CD40L interaction only acts to stimulate any type of naive T cells?
Yea the confusion is deep with this one or I’m just uncertain as to what I’ve read and I have yet to do any q-banks…