Hey guys just wondering with autoimmune diseases which aspect of the immune system is destroying the self cells, the cytotoxic T cells or the B cells and antibodies? Also how are eukaryotic pathogens destroyed? I assumed the phagocytes would be too small to engulf them thus agglutination would be ineffective.
With autoimmune diseases, cytotoxic T-cells are primarily involved. Of course, helper T-cells activate cytotoxic T cells to act on self cells. Cytotoxic T-cells release perforin (a cytotoxic protein) that punches holes through the plasma membrane of these self cells, resulting in these cells lysing.
Hey I've got a few questions
* Upon second encounter with a particular pathogen, I know the immune response is much faster and greater due to the presence of B-memory cells which recognize the antigen and know exactly which antibodies to create. But exactly how does the presence of B-memory cells speed up the rate and strength of the response? Does it mean that there is no need for plasma cells to undergo proliferation?
*And also, I came across a question asking why mast cells are perceived to play a positive role in the inflammatory response, but a negative role in hypersensitivity reactions.
I'm aware of their role in allergic response, but unsure of how they aid the inflammatory one.
*Finally, is the action of mast cells specific or non-specific?
Thanks guys 
I'll start off with your last question. You cannot really ask whether a mast cell is specific or non-specific. It really depends on the situation it is involved in. For instance, mast cells, which are found on the lining of blood vessels, release histamine during an inflammatory response to attract phagocytes to the infective area. In this instance, it is non-specific. Why? Mast cells release histamine to attract phagocytes irrespective of the types of pathogens that have penetrated the internal environment of the organism. However, when looking at hypersensitivities against allergens, the IgE antibodies that bind to the outer surface of these mast cells having paratopes (antigen binding sites) specifically complementary to the shape of the antigens of a specific allergen that the individual is sensitised to. In this instance, it is specific (adaptive). Why? Because mast cells will ONLY release histamine when a specific allergen that the organism is sensitised to binds to the IgE antibodies, which are in turn bound to the outer membrane of the mast cells.
Next point: mast cells release histamine during the inflammatory response to attract phagocytes to the infective area, resulting in the phagocytosis of non-self, pathogenic matter, to prevent the spread of infection. However, in allergic responses, the release of histamine by mast cells causes profound, emphatic and dramatic responses to the detected allergen, including constriction of airways, itchiness, swelling, excessive production of mucous, etc. So that's how you can have mast cells acting positively in one instance, and not so positively in the other. Again, depends on the situation itself.
Memory B-cells retain immunological memory of the antigenic markers of the specific pathogen that the individual is now actively immunised against. When the pathogen is encountered on a subsequent occasion, there is no need for clonal selection. That is, clonal expansion (involving the rapid proliferation of B cells which differentiate into memory and plasma B cells that secrete specific immunoglobulins) occurs at an earlier time than when the individual first encountered the pathogen, because of the delay in the time required for the surface antibodies of a SPECIFIC B-cell to bind to the complementary antigenic marker of a pathogen, to then actually activate that B-cell to rapidly proliferate. The presence of memory just really speeds up the process by which a higher concentration of antibodies (in terms of humoral immunity) are produced, to elicit a more emphatic, rapid response to that specific pathogen.
Hope this helped!
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