@@animatedbiologywitharpan if the subset of t helpers(viz th1,th2,th17 etc )decides the Ig to be released, by the thier specific cytokines released to the B cell(antigen presenting),then how could we say, In primary infection,Ig M will be more and in 2ndry infection IgG will be more in serum? ie,if Th1 is the helper subset formed,would it only cause for IgG producing effector B cell synthesis,so from the first occurance of that infection,IgG may be the main Ig in serum.Is this possible sir?
Tomorrow in my immunology exam... The videos of ARPAN DADA... are so easy and lucid to understand that it boosts my confidence level.. 😅 Thank you DADA for ur lovely animated video's.
Your videos are just amazing🙌😀 Difficult topics explained in such an easy way. Sometimes it becomes difficult to visualise all the text we have read in books but ur videos made it easy for me Thank you❤️ Great job, keep up the good work👍
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Please share my channel link with your friends and help me to reach big audience . Don't forget to check out all my playlists. Wide collection of immunology videos are there.
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So there is a question. After the AID enzyme comes into action, what really recruits the repair enzyme? And why not any other repair enzyme with high fidelity?
thank you for amazing explanation. you mentioned B cell isotype switching is antigen dependent and requires mhc 2 cd40 co stimulation so can we say its also t cell dependent ? is this the case where polysaccharide and conjugated vaccines differ ? polysaccahride vaccines activate b cells indepent from t cells so no somatic hypermutation and generation of high affinity antibodies and ig G thats what i understand
T cell stimulates strong b cell activation which is a prerequisite for isotype switching. Moreover, T cells provide essential cytokine signals, such as IL-4 and IL-21, which direct B cells to undergo isotype switching, resulting in the production of antibodies with different effector functions. This T cell-dependent process enhances the adaptability and effectiveness of the immune response.
Thank you sir for the video❤i have a question please: so if i understood, isotype switching happens to the Ab produced not the BCR and one B cell either makes igM or IgD or IgE or IgA or IgG right ?
NF-κB and STAT1 regulate B cell class switching: NF-κB activates AID for DNA recombination, crucial in antibody class change. STAT1 responds to interferons, promoting IgG2a and IgG3 production in infections. Both transcription factors coordinate immune responses, ensuring effective antibody diversification against pathogens.
Why is isotope switching occur ? It only changes the conserved heavy chains which don’t bind to pathogens only to the own B cells, so why do we need different types of conserved regions if they don’t select for pathogens ?
Since the variable region does not change, class switching does not affect antigen specificity. Instead, the antibody retains affinity for the same antigens, but can interact with different effector molecules. Example : IgM interacts with complement better than others...IgG is better in terms of crossing placenta etc.
When the naive B cell encounters a pathogen, is this with the help of the dendritic cell traveling to the lymphoid with parts of the pathogen covering it? Or does the pathogen make its way to the lymph, and the B cell directly recognizes it and takes a piece from it?
As far as I know both no affinity and high affinity get destroyed by negetive selection and only T cell with low affinity survives through positive selection
@@animatedbiologywitharpan OK but please make a video on those 3 phases of Tifr interview.BTW video was very helpful for my upcoming gat b exam and all thank you.
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I have a question regarding the naive B cell . So it can produce IgM and IgD without encountering a pathogen ? But why does they use IgM and IgD levels to see if the patient has immunity to a specific disease?
Very good question....let me tell you that with all infection it's not true that there would be class switching as a result only IgM could be produced.Now b cell has IgM by default but its membrane bound ,after infection secreted IgM is synthesized which is specific to the antigen coming from a bacteria let's say.
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Really glad to know it was useful. Please follow my instagram page and facebook page. Please share my youtube channel link with your friends and help me to reach big audiance
Really glad to know it was useful. Please follow my instagram page and facebook page. Please share my youtube channel link with your friends and help me to reach big audiance
Could you please help me by sharing my contents with your friends group/ college group. I put huge efforts in making these videos but unfortunately not a lot of people are watching this.
Amazing man, that´s a perfect review of a theme that takes a long time to understand!
Please check out my entire immunology playlist and share my channel link with your friends
A tip : watch movies at flixzone. I've been using it for watching a lot of movies these days.
@Briar James Yup, have been watching on flixzone} for since december myself :D
@Briar James Yup, been watching on Flixzone} for since december myself =)
This is the best explanation I could ever found .. thank you
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Thank you, sir Arpan. I am a medical student who tries to understand immunogenetics and your channel is the best thing I could hope for
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@@animatedbiologywitharpan if the subset of t helpers(viz th1,th2,th17 etc )decides the Ig to be released, by the thier specific cytokines released to the B cell(antigen presenting),then how could we say,
In primary infection,Ig M will be more and in 2ndry infection IgG will be more in serum?
ie,if Th1 is the helper subset formed,would it only cause for IgG producing effector B cell synthesis,so from the first occurance of that infection,IgG may be the main Ig in serum.Is this possible sir?
I have immunology exam tomorrow. This is so helpful and lucid to understand. Thank you 😊
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Glad to know that my connect is useful
Amazingly explained in detail 🙂 very easy language gud teaching helps me to better undertood I really liked this video plz keep doing👍
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@@animatedbiologywitharpan sure definitely 👍
Thank you very much. Now the concept is more clear
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Tomorrow in my immunology exam...
The videos of ARPAN DADA... are so easy and lucid to understand that it boosts my confidence level.. 😅
Thank you DADA for ur lovely animated video's.
All the best for your exam
3 more days for me. I also enjoy the content alot! Greetings from germany
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I Tutor organic chem. For next Semester Preperation i will mention you 🙏
@@kevinbenjaminbassler9530 that would be very kind of you. Thanks in advance
Thank you. I was searching our University library, and nothing was so concise as this.
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Even after working really hard I can't reach s lot of viewers
@@animatedbiologywitharpan certainly 👌
Truly an incredible explanation Arpan! I was finding it so difficult until I saw your video.. Thank you very much and take care!
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thank you so much, I'm a french med student, it was a very difficult topic to me
but you explained it in an easy way. :)
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Salute to your art sir.... Your are great and intellegent teacher... I always search for your videos if I need any topic
glad to hear from you....thanks a lot for the complement
Amazing ! Thanks to you i've understand in time for my exam this notion ! It is very well explained thank you !
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Your videos are just amazing🙌😀 Difficult topics explained in such an easy way. Sometimes it becomes difficult to visualise all the text we have read in books but ur videos made it easy for me Thank you❤️ Great job, keep up the good work👍
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Such a great explanation ❤️🔥
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Excellent i just understand each and every detail clearlt
th-cam.com/channels/4IpyopsGWSjaPACNTZLuqg.html please subscribe to my second channel as well
koszonom szépen from Hungary
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Cool work man , clear and clean keep up
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Amazing!
I shared the link with my friends in the faculty although we speak Arabic but the explanation deserves
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Wonderfully explained sir 🙏🙏🙏🙏🙏
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@@animatedbiologywitharpan sure sir 🙏🙏.
Thank you for the great explanation 😢
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Very nice and basic explanation
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This is soooooooo good.
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Awesome explanation
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Amazing explanation!!
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Nice explanation..👍
shubham kr rai please share my channel link with your friends and colleagues
Very well explained !!❤️
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@@animatedbiologywitharpan Sure❤️
THANK YOU FOR THIS AMAZING VIDEO
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Amazing video👍🏻
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@@animatedbiologywitharpan of course! Keep up the great work👍🏻
This video is amazing. Thank you so much!!
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Excellent lecture
structured immunology playlist th-cam.com/play/PLKtiwIJ8Q7rq77W7r4cXPrbhi_VpLWw8c.html&si=qSHBfEJ6fvW_8dYU
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Great video!!
Woooooooow nice explanation
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explained in details !!
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Wow amazing you explain in detail,what do you prefer to prepare for content
Kuby immunology
Thank you so much, very informative
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So there is a question. After the AID enzyme comes into action, what really recruits the repair enzyme? And why not any other repair enzyme with high fidelity?
If you will go in more and more detailing you will get a pH, ions presence, and many many other factors 😑
thank you for amazing explanation. you mentioned B cell isotype switching is antigen dependent and requires mhc 2 cd40 co stimulation so can we say its also t cell dependent ? is this the case where polysaccharide and conjugated vaccines differ ? polysaccahride vaccines activate b cells indepent from t cells so no somatic hypermutation and generation of high affinity antibodies and ig G thats what i understand
T cell stimulates strong b cell activation which is a prerequisite for isotype switching. Moreover, T cells provide essential cytokine signals, such as IL-4 and IL-21, which direct B cells to undergo isotype switching, resulting in the production of antibodies with different effector functions. This T cell-dependent process enhances the adaptability and effectiveness of the immune response.
hi, class switching can also occur before germinal center formation
Thank you sir for the video❤i have a question please: so if i understood, isotype switching happens to the Ab produced not the BCR and one B cell either makes igM or IgD or IgE or IgA or IgG right ?
ya soluble anyibodies are generated and constant regions are changed
Excellent !
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Incredible!
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Amazing man!!!
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I have a doubt. The region where NK-kb and Stat1 bind , in that region is the AID recruited? I can't understand this part. Plz help me
NF-κB and STAT1 regulate B cell class switching: NF-κB activates AID for DNA recombination, crucial in antibody class change. STAT1 responds to interferons, promoting IgG2a and IgG3 production in infections. Both transcription factors coordinate immune responses, ensuring effective antibody diversification against pathogens.
@@animatedbiologywitharpan ok thank you
Why is isotope switching occur ? It only changes the conserved heavy chains which don’t bind to pathogens only to the own B cells, so why do we need different types of conserved regions if they don’t select for pathogens ?
Since the variable region does not change, class switching does not affect antigen specificity. Instead, the antibody retains affinity for the same antigens, but can interact with different effector molecules. Example : IgM interacts with complement better than others...IgG is better in terms of crossing placenta etc.
damit man, you content is lit👊👍
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@@animatedbiologywitharpan sure man👍.
When the naive B cell encounters a pathogen, is this with the help of the dendritic cell traveling to the lymphoid with parts of the pathogen covering it? Or does the pathogen make its way to the lymph, and the B cell directly recognizes it and takes a piece from it?
Dendritic cells take the antigen and move towards the lymph node
THANK YOU SOME MUCHE YOU HAVE AMAZING EXPLAINE
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Good lecture but B cells mature in bone marrow only and not in lymph node, I believe
No, maturation doesn't take place in bone marrow, it's always in the lymph node
As far as I know both no affinity and high affinity get destroyed by negetive selection and only T cell with low affinity survives through positive selection
Can you make a video on carrier options after msc from any life science stream in future?
th-cam.com/channels/4IpyopsGWSjaPACNTZLuqg.html my second channel would deal with all of these topics
@@animatedbiologywitharpan OK but please make a video on those 3 phases of Tifr interview.BTW video was very helpful for my upcoming gat b exam and all thank you.
Thank you!
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I have a question regarding the naive B cell . So it can produce IgM and IgD without encountering a pathogen ? But why does they use IgM and IgD levels to see if the patient has immunity to a specific disease?
Very good question....let me tell you that with all infection it's not true that there would be class switching as a result only IgM could be produced.Now b cell has IgM by default but its membrane bound ,after infection secreted IgM is synthesized which is specific to the antigen coming from a bacteria let's say.
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you're amazing! ty!
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Thank you sir ❤
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Thank you so much! Btw which program did you use to film your display?
Obs studio
So class switching is simply T dependent activation ?
Class switching happens in B cells but not in T cells. if there is no strong T cell dependent B cell activation then class switching would not happen
@@animatedbiologywitharpan wow that was a quick response ,thank you so much for clarifying it
Hello is interferon y secretion is required for all the antibody isotypes or is it only for igg
IFN-gamma inhibits the secretion of IgG3, IgG2b, IgG1, and IgE, and enhances the secretion of IgG2a.
Amazing !!!!!!
Thanks a lot.
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Can you please provide a reference for this video?
Kuby immunology 7th edition
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Thank u so much
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Much appreciated ❤️❤️❤️
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Sir,May you please tell me if pathfinder is sufficient for csir NET JRF LIFESCIENCE Immunology portion along with some TH-cam vedios.
When CSIR NET is concerned I would suggest Kuby immunology
thank you
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Thank you for your video! Can hyper IgM syndrome generate IgD?
Nope its not possible in my opinion
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@@animatedbiologywitharpan Sure! Thank you for your efforts!
you are amazing
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Do different cytokines all lead to STAT activation?
Yes they do
Great video but the sound was not too good.
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Well done bro.
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Nice
Thanks
❤️
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🙏❤️❤️❤️❤️
Allah yihmeek.
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Can you please improve the audio quality? Its horrible
Thanks for this suggestion....I will try to improve the quality in subsequent videos.
Arpan the GOAT
I don't understand any context of your comment.
@@animatedbiologywitharpan don't worry, it means you're the Greatest Of All Time 🐐 for making Immunology make sense 😎
Ok now I understand....
Quite funny...please share my channel link with your friends
Thank you sir ❤
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