Summary of B and T cell memory
Transcript for B and T cell memory
B and T cell memory
Key features of the innate immune response are that the cells are non-specific, meaning that they don’t distinguish one invader from another invader, the response is really fast - occurring within minutes to hours, and there’s no memory associated with innate responses.
The adaptive response, which is mediated by lymphocytes like B and T cells - is the opposite of the innate immune response.
B and T cells have unique receptors - the B cell receptor and T cell receptor - that differentiate pathogens from each other using their unique parts - called antigens.
These receptors are developed while the T cell or B cell is developing in the bone marrow for B cells or thymus for T cells.
Once the cell has a unique antigen-specific receptor expressed on its surface it begins traveling through the lymphatic system - passing through lymph nodes in search for the one antigen that fits the receptor perfectly.
If they encounter that antigen, a signal gets delivered to the cell’s nucleus that lead to clonal expansion.
That’s where a single T cell or B cell replicates over and over - creating an army of clones that can combat the pathogen.
Once the immune response is complete, many of these cells die by apoptosis restoring the immune response to its original size - with one major change.
Some of the B and T cells become memory cells, which are basically a pool of lymphocytes that are all set to combat the pathogen, if they encounter it again!
Immunologic memory is sometimes referred to as a secondary or anamnestic response, and it’s different from the primary response.
During the primary response a small number of naive B and T cells require activation before they can respond to the pathogen.
And activating those B and T cells requires a relatively high pathogen burden and can take days to weeks.
And the innate response is really important to fill the gap while the adaptive response is being mounted.
In the secondary response, the memory B and T cells, as well as antibodies, are already made, and it takes a relatively low pathogen burden to re-engage the adaptive immune response.
As a result, the innate and adaptive immune response end up working with each other right away to eliminate the pathogen.
In the primary immune response, B cells get activated through their interactions with other immune cells.
First, special dendritic cells called follicular dendritic cells trap antigens for the B cells and send out stimulatory cytokines.
Then, the B cell acts as an antigen presenting cell - serving up antigen to T follicular helper cells.
In response, the T follicular helper cell expresses CD40L on its surface and produces IL-21, and together they induce the B cell undergo class switching.
In class switching, the B cell shifts from expressing a B cell receptor with IgM and IgD to expressing IgG, IgE, or IgA.
Some of these B cells go on to become memory B cells.
That means that the memory response is limited to peptide antigens which can be seen by T cells.
And that T cell-independent antigens like lipids and carbohydrates don’t lead to memory B cells.
It also means memory B cells don’t produce IgM and IgD.
Memory B cells live for up to 10 years in a lymph node, and they often differentiate into IgG secreting plasma cells when they get reactivated.
Now, because of somatic hypermutation, IgG antibodies created toward the end of the primary immune response typically have higher affinity than the IgM antibodies created early in the primary immune response.
These high affinity IgG antibodies therefore bind to Fc gamma receptor II on newly activated IgM producing B cells, inhibiting them from differentiating into plasma cells.