medicowesome
medicowesome:

immense-immunology-insight:

Thymus dependent activation of B lymphocytes simplified
"Activation makes the B cell a hero & bestows new responsibilities to it."
Why does the B cell need to be activated? (Click here to read from the previous post.)To generate sufficient quantities of effector lymphocytes. Only lymphocytes with the appropriate receptor specificity (The one who recognizes the enemy properly) must be activated & allowed to proliferate.B cells require two distinct signaling events for activation.Signal 1 is generated when multivalent antigen binds and cross links the B cell receptor (BCR).(Cross-linking is like holding a piece of paper with both hands. It’s the same paper but different parts that your are holding. Your hands are the B cell receptors & the paper is the antigen.)After signal 1, various cytokines and ligands on the B cell membrane provide signals for progression.The antigen is internalized and processed into peptides for display on MHC class II molecules.(Now that your hands are together, you start making a flag. The stick of the flag is the MHC molecule.)


Antigen binding also initiates signaling through the BCR that induces the B cell to up-regulate a number of cell-membrane molecules, including class II MHC molecules and the co-stimulatory ligand B7.
(You are the childish naive B cell who got a proper paper for the first time. So along with the flag, you do some extra origami, just in excitement.)


Increased expression of these membrane proteins increases the ability of the B cell to function as an antigen-presenting cell.
(All that origami makes you stand out, you are awesome in presenting your craft.)

Because of this, the B cell is able to present antigen to TH cells at antigen concentrations that are 100 to 10,000 times lower than what is required for presentation by macrophages or dendritic cells.
(You get the T helper cell’s attention easily this way & wave the flag.)

Once a TH cell recognizes a processed antigenic peptide displayed by a class II MHC molecule on the membrane of a B cell, the two cells interact to form a T-B conjugate.
(The T cell & you are like buddies now. Look at you, making all friends and stuff :P )


Formation of a T-B conjugate leads to the release of TH-cell cytokines & up-regulation of CD40L.
(Your friendship helps the T cell to make gifts for you.)


Signal 2 is generated when CD40L interacts with CD40 on the B cell.
(The gift was a secret signal.)

Signal 2 along with signal 1 drives the B cell into G1 phase.
(G0 is the sleepy phase, you go to the G1 phase which makes you active and awake.)


The activated B cell begins to express receptors for cytokines, such as IL-2, IL-4 & IL-5. (You make more stuff!)
These receptors then bind the cytokines produced by the interacting TH cell. (You get more gifts!)

The signals produced by these cytokine-receptor interactions support B-cell proliferation and can induce differentiation into plasma cells and memory B cells, class switching, and affinity maturation. 


(The exchange of gifts help you to do the following things - )

B cell proliferation: Making clones of yourself.
(You are a hero & it’s good to have more heroes like yourself around for help.)

Differentiation into plasma cells, which secrete lots of antibodies.
(Antibodies are like paper clips, they can pin to paper.)

Differentiation into memory B cells that remember the event.
(You make sure some of your clones have photographic memory, in case you see a similar paper in the future.)

Class switching which is changing the B cell’s antibody production from one isotype to another.
(It’s like making different kinds of paperclips, for different uses.)

Affinity maturation which increases the affinity for the antigen.
(It’s like perfecting the paper clip.)

That’s all!
Thank you for reading :)
-IkaN

Clinical correlates:
Bruton’s X-Linked Agammaglobulinemia: It is due to a failure in signal transduction and B-Cell Development. The signaling events required for activation are defective, so no antibody is produced at all.
X-linked hyper-IgM syndrome: TH cells fail to express CD40L. Patients produce IgM but not other isotypes. Such patients fail to generate memory cell populations, fail to form germinal centers, and their antibodies fail to undergo somatic hypermutation.

medicowesome:

immense-immunology-insight:

Thymus dependent activation of B lymphocytes simplified

"Activation makes the B cell a hero & bestows new responsibilities to it."

Why does the B cell need to be activated? (Click here to read from the previous post.)
To generate sufficient quantities of effector lymphocytes. Only lymphocytes with the appropriate receptor specificity (The one who recognizes the enemy properly) must be activated & allowed to proliferate.

B cells require two distinct signaling events for activation.

Signal 1 is generated when multivalent antigen binds and cross links the B cell receptor (BCR).
(Cross-linking is like holding a piece of paper with both hands. It’s the same paper but different parts that your are holding. Your hands are the B cell receptors & the paper is the antigen.)

After signal 1, various cytokines and ligands on the B cell membrane provide signals for progression.
The antigen is internalized and processed into peptides for display on MHC class II molecules.
(Now that your hands are together, you start making a flag. The stick of the flag is the MHC molecule.)

Antigen binding also initiates signaling through the BCR that induces the B cell to up-regulate a number of cell-membrane molecules, including class II MHC molecules and the co-stimulatory ligand B7.
(You are the childish naive B cell who got a proper paper for the first time. So along with the flag, you do some extra origami, just in excitement.)
Increased expression of these membrane proteins increases the ability of the B cell to function as an antigen-presenting cell.
(All that origami makes you stand out, you are awesome in presenting your craft.)
Because of this, the B cell is able to present antigen to TH cells at antigen concentrations that are 100 to 10,000 times lower than what is required for presentation by macrophages or dendritic cells.
(You get the T helper cell’s attention easily this way & wave the flag.)
Once a TH cell recognizes a processed antigenic peptide displayed by a class II MHC molecule on the membrane of a B cell, the two cells interact to form a T-B conjugate.
(The T cell & you are like buddies now. Look at you, making all friends and stuff :P )
Formation of a T-B conjugate leads to the release of TH-cell cytokines & up-regulation of CD40L.
(Your friendship helps the T cell to make gifts for you.)
Signal 2 is generated when CD40L interacts with CD40 on the B cell.
(The gift was a secret signal.)
Signal 2 along with signal 1 drives the B cell into G1 phase.
(G0 is the sleepy phase, you go to the G1 phase which makes you active and awake.)
The activated B cell begins to express receptors for cytokines, such as IL-2, IL-4 & IL-5. (You make more stuff!)
These receptors then bind the cytokines produced by the interacting TH cell. (You get more gifts!)
The signals produced by these cytokine-receptor interactions support B-cell proliferation and can induce differentiation into plasma cells and memory B cells, class switching, and affinity maturation. 
(The exchange of gifts help you to do the following things - )
B cell proliferation: Making clones of yourself.
(You are a hero & it’s good to have more heroes like yourself around for help.)
Differentiation into plasma cells, which secrete lots of antibodies.
(Antibodies are like paper clips, they can pin to paper.)
Differentiation into memory B cells that remember the event.
(You make sure some of your clones have photographic memory, in case you see a similar paper in the future.)
Class switching which is changing the B cell’s antibody production from one isotype to another.
(It’s like making different kinds of paperclips, for different uses.)
Affinity maturation which increases the affinity for the antigen.
(It’s like perfecting the paper clip.)
That’s all!
Thank you for reading :)
-IkaN

Clinical correlates:

Bruton’s X-Linked Agammaglobulinemia: It is due to a failure in signal transduction and B-Cell Development. The signaling events required for activation are defective, so no antibody is produced at all.

X-linked hyper-IgM syndrome: TH cells fail to express CD40L. Patients produce IgM but not other isotypes. Such patients fail to generate memory cell populations, fail to form germinal centers, and their antibodies fail to undergo somatic hypermutation.

  1. theesakizzie reblogged this from immense-immunology-insight and added:
    if you get this, then we can be best friends. but probs not. I can only dream
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    i love everything about this
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    B cell activation explained in the manner of an excited child… With their first piece of paper… Oh and cloning...
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