Can anyone explain step-by-step on how innate and adaptive immune system respond to a bacteria and a virus? In order of what happens first please!
Thanks beforehand!
Innate
Okay so the innate system responds the same way to both bacteria and viruses- it's non-specific.
Firstly mast cells release histamine. Histamine binds to capillary walls and causes vasodilation (expansion). This causes more blood to go to the area, which causes heat & redness. Histamine also causes capillary walls to become 'leaky' - white blood cells are able to cross the membrane to access the infected area - this causes swelling.
Some of those white blood cells are phagocytes. Neutrophils are an innate phagocyte. They will travel through the area and phagocytose ('eat') anything that is non-self. Macrophages and dendritic cells are also phagocytes however they are also Antigen Presenting Cells (APC's). They will phagocytose foreign material and then use it to trigger the adaptive immune response.
Also part of the innate immune response are complement proteins. Complement are actually a group of proteins that perform 3 functions.
1. Aid phagocytosis by opsonizing antigens. Basically they make it easier for phagocytes to find antigens - you don't need to know how.
2. Trigger inflammation by attracting neutrophils and macrophages to the area.
3. Form a Membrane Attack Complex - they make holes in bacterial cell walls.
Because of 3. they are most effective against bacteria.
Humoral (extracellular)
This actually occurs for both bacteria and viruses, but if you get a question on viruses you should talk about intracellular immunity.
Humoral immunity involves B cells, and to a lesser extent T helper (Th) cells.
When pathogens are floating throughout the body, bits of them will inevitably break off. These bits are called free antigens, they will end up encountering a naive B cell that can bind to them. When this happens that B cell is said to be 'selected'.
At the same time a macrophage or dendritic cell that has engulfed a pathogen back in the innate immunity stage will present the antigens from that pathogen on its MHC2 markers. It will then travel throughout the body until it find a naive T helper cell that it can bind to. When this happens that Th cell is 'selected'.
The selected B cell and Th cell travel throughout the body trying to find each other. When they do find each other, the B cell will present the antigen it found to the Th cell. If the Th cell can bind to it then they have the same specificity (they've bound the same antigen). The Th cell will release cytokines (a type of signalling molecule). These cytokines stimulate both the Th and B cell (and cytotoxic T cells in cell-mediated immunity) to divide (make copies) and differentiate (into memory cells and active Th/Plasma B cells). Memory Th and B cells stay in the body to fight against any subsequent infection by a pathogen with an identical antigen. The active Th cells will continue to bind antigens from macrophages and dendritic cells. I'm not entirely sure what the purpose of this continuing is - I believe it has something to do with knowing when to stop the immune response? We don't need to know the details for VCE though Plasma B cells make lots and lots of antibodies with the same antigen specificity (shape of their binding site) as the B cell receptors that bound the initial antigen (these receptors are actually antibodies). These antibodies are released and travel throughout the body binding to any complementary antigens they find.
This has a few purposes.
1. It makes the antigens easier for phagocytes to find.
2. It stops virus antigens from entering cells - it makes them too large
3. It can cause agglutination (clumping). Antibodies have 2 identical receptors so they can bind to two antigens and create a clump.
Cell mediated (intracellular)
Cell-mediated immunity involves cytooxic T cells, and to a lesser extent T helper cells.
This only happens with intracellular infections, as well as cancer, transplantation, and autoimmune responses.
Cytotoxic T (Tc) cells regularly travel throughout the body attempting to bind to peptide fragments presented on MHC1.
MHC1 is found on all cells that have a nucleus - that is, all cells except red blood cells. During normal peptide production, fragments are presented to check that they are self - to check that there is no virus or mutations.
When a Tc cell successfully binds to one of these fragments it is 'selected'. The Tc cell will release granzymes (including perforin) that induce apoptosis in the affected cell. When the cytokines from humoral immunity are released by the T helper cell, the Tc cell will divide and differentiate into memory Tc cells, which remain in the body to kill any cell that presents an identical peptide fragment at a later date and active Tc cells. These active Tc cells will have the same antigen specificity (the same shaped receptor) and will travel throughout the body and kill any cells they find that are presenting the same peptide fragment.
I wasn't really sure what you know so I've probably over explained some parts, let me know if any of that doesn't make sense.
In terms of timing Innate occurs first, adaptive overlaps innnate. Humoral and cell-mediated can start in either order but cell-mediated cannot truly occur until cytokines are released from the T helper cell.
@everyone let me know if I messed any of that up