Review of B cells, CD4+ T cells and CD8+ T cells. Created by Sal Khan.
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Hold up, isn't it also the case that MHC expression is DECREASED on infected/cancerous cell membranes? It's not just that they present some molecule that targets them for destruction. Or is that where NK cells come in?
Thank you..thank you..thank you SOOO MUCH!!I'm a med-student in my 4rth year..I read somewhere in pathology that B cells produce antibodies..so when my microbiology teacher asked which cells produce antibodies and I replied B cells he just disagreed soooo strongly and said plasma cells is the answer..which I also knew but why not B cells which I read in pathology?!..I didn't get where I was wrong..but your vedio explained that effector B cells and plasma cells are same..That answers all my questions..Thank you so much to you and to your wife for mentioning that out😊..It was bugging me like hell😪
cd8 cytotoxic t cells are called T-killer cells; another CD8 are the T-supressors(they suppress the B-cell proliferation) and the variation T-helpers that interact with the hemopoetic stem cells and control differentiation and proliferation are called T-amplificators
Are u Google? U know every thing . U know biology u know physics u know chemistry you know geogra, social studies ... blabla bla ... i m so jealous. How do u manage to keep all the stuff in your mind .. are you a modern living encyclopedia! 😅😨
Thank you, that was really helpful! I am taking Anatomy and Physiology online and have been struggling to understand the lymphatic system because it is kind of obscure without a visual, but your videos have really helped me along.
HIV is a retrovirus that creates an autoimmune (fighting oneself) response that inactivates T helper cells, therefore the immune system is unable to tag foreign invaders and "sound the alarm" through the process explained in the video. Most individuals with HIV don't acquire AIDS and pass because of the HIV itself, its from some other opportunistic infection that was made possible due to the lack of CD4 (helper T) cells. Great question! -D.C. student
If I'm not mistaken, you say "plasma cells" as the cells that produce antibodies as they are the activated form of B cells. You're technically not wrong if you say B cells but they have to undergo cell activation to produce antibodies and thus, in that activated state, they're known as plasma cells.
we guys learn from this better than university cause we are here by choise and in uni we are kind of bound to. most you who are watching this have an exam tomorrow, you are giving your full attention here, but on the class day, well, i think you know how attentive you were on class day. Dont just blame the teachers....
on the note, i also have an exam :p
I have a question that keeps bugging me because I cant find any answer to this. From what I understand T helper cell gets activated when its receptors recognize antigens presented by MHC II on some APCs. What's not clear to me is that when the activated T helper cell move on to activate B cells, does it require the B cells to have the same antigen presented on its surface just like the APC has presented in order for the B cell to produce antibodies against that specific antigen? If not, how would the T helper cell instruct the B cells what antibody to make? If yes, the chance for all events to happen seems to be very very small to me. Can someone please answer my questions? It would be a great help to me. Thanks
Correct. That is why if you want humoral immunity (antibody production) you need at least 2 antigens present in the blood: one that is read by the B cell, and the other that is read by the helper T cell, and then those B and T cells need to bump into one another.
This is why immunity is somewhat of a numbers game with the number of antigens and WBC's. The body is more likely to respond faster to more antigens present in the blood, simply because it is more likely that two activated B and T helper cells bump into each other.
question: so the T helper cell that activates the B cell when it bind to the MCH II ... does that T helper cell HAVE to be activated already? can it be a naive T helper cell that is specific for that MCH II antigen? thanks to anyone who can help me :)
cytotoxic T cells attacks endogenously synthesized antigens right ? Does that mean after a virus enters the cell, when it takes over the machinery of the cell, then it starts producing viral proteins..so these viral proteins are presented to Tc cells right ?
you don't know what does your wife study ?!
it's a crime man, i'm wondering about her reaction when watching the video :D
remembered me of "Gone Girl" film, when the hot-police officer told him "you don't know your wife's blood type
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Thank you for this. It really explained pretty much everything I have taken in my immunology course so far. However, I wonder why you haven't mentioned NK cells. It is a part of the innate system that has it own mechanism. I guess I'll just look it up somewhere else.
There are infact 3 types of T cells 1) Cytotoxic T cells CTL (CD8+) cells 2) T-helper cells (CD4+ Cells) and 3) T-regulatory cells also know as suppressor T cells or Treg (FOXP3+ CD25+). Treg cells are very important cells because they are required to suppress activation self-reactivity, and prevent autoimmunity.
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Performance of A-shares.
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Current Dividend Preference.
Participating Preferred Stock.
Convertible Preferred Stock.
Cumulative preferred stock includes a provision that requires the company to pay preferred shareholders all dividends, including those that were omitted in the past, before the common shareholders are able to receive their dividend payments.
Non-cumulative preferred stock does not issue any omitted or unpaid dividends. If the company chooses not to pay dividends in any given year, the shareholders of the non-cumulative preferred stock have no right or power to claim such forgone dividends at any time in the future.
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Significance to Investors.