t cells Flashcards
t cell role in immune sytsem
activation of naïve T cells requires them to encounter a specific antigen, results in rapid proliferation (known as clonal expansion), and results in both effector cells and memory cells. CD4 T cells in particular can also acquire distinct functional capacities (or helper functions) that promote distinct parts of the immune system. For instance cells that become Type 1 helper cells (or Th1 cells) produce molecules that promote control of intracellular pathogens. Look at the other CD4 T cell subsets and note the different immune responses they participate in.
what is Type I hypersensitivity
is an allergic reaction provoked by re-exposure to a specific type of antigen referred to as an allergen
what type of antibodies mediate the response
IgE
why do non allergic people make IgE
Non-allergic individuals predominantly only make IgE in response to parasitic infections or very potent venoms
worst sort of antibodies do
produce antibodies against common multivalent (which means the antigen has multiple sites at which an antibody can attach or antigen can be produced) environmental antigens
describe a test used for testing allergies
Skin prick tests. Exposing the skin to small amounts of allergen can often be used to diagnosis allergy.
what is the end result of the allergy
The end result, however, is the generation of type 2 helper CD4 T cells and B cell helper follicular CD4 T cells which produce the type 2 cytokines IL-4 and IL-13; when these act on B cells they can promote B cell to switch to producing antigen specific IgE
what il act on b cells to produce IgE
il 4
il 13
is IgE found in circulation
IgE is very rarely found in the circulation, even in allergic individuals
what happens to teh IgE on the im
IgE is rapidly bound to the surface of innate immune cells
granulocytic cells express a high affinity IgE receptor, Fc epsilon receptor I
If an allergen is encountered by cell bound IgE it results in rapid crosslinking and degranulation of the mast cell or basophil.
what is the early phase
bioactive small molecules produced directly by mast cells, occurs within minutes of allergen exposure
A later response
often seen within a few hours is the result of the recruitment of early inflammatory cells such as neutrophils.
A third phase, or late response
is often peaks 3-4 days after exposure where high frequencies of eosinophils are recruited and Th2 cells are present
.
Type II hypersensitivity
antibody-mediated cytotoxic hypersensitivity, involves the destruction of cells by IgG or IgM antibody bound to antigens present on the surface of the cells
example of type 2 hypersensitivity
mismatched blood transfusion could be considered one such hypersensitivity with antibodies recognising different, non-self, carbohydrate groups of the transfused red blood cells resulting in immune induced destruction of those red blood cell, inflammation and tissue damage.
type 2
As can be inferred from the examples above type II sensitization can involve either exposure to a foreign antigen (for example some drugs can bind to the surface of cells in the blood, or non-self antigens blood transfusions or organ transplants) or the aberrant response to a self-antigen resulting in IgGs or IgMs that recognise cell surface structures.
antibody diseases
Anti-receptor activity – blocking or activating its function
Antibody dependent cell-mediated cytotoxicity (abbreviated to ADCC)
Classical activation of the complement cascade
complement cascade is what
is a complex process by which antibody on the surface of cells is recognised by the complement components, ultimately leading to the formation of the membrane attack complex (MAC) in the surface of the cell, and cell death due to loss of osmotic integrity
what can the cc result in
inflammation, opsonisation and recruitment and activation of immune cells.
the ADCC antibody-antigen complexes on the surface of cells are bound by Fc receptors are found where
expressed by cells such as granulocytes and NK cells
result in
inflammatory mediators, chemokines and cytokines.
summary result of type 2
Type II hypersensitivity therefore can result in multiple mechanisms of tissue injury including local or systemic inflammation, cell depletion leading to a loss of function or imbalance in organ function.
what is type 3
Type III hypersensitivity is sometimes known as immune complex driven disease
immune complexes are what
Immune complexes are non-cell bound antigen-antibody complexes which are normally cleared through the activity of the immune system
what can happen of immune complexes are not cleared
the immune complexes end up being deposited in the blood vessel walls and tissues, promoting inflammation and tissue damage
results in what
fever, rashes, joint pain or protein in the urine: vasculitis if deposited in blood vessels, glomerulonephritis if in the kidneys or arthritis if in the joints. Many auto-immune diseases including rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus (SLE) involve type III reactions
Type IV hypersensitivity
, other known as delayed-type or T cell mediated hypersensitivity, is primarily initiated by T cell
how it works
a sensitization phase needs to occur where antigen is presented to naïve T cells by antigen presenting dendritic cells, resulting in the generation of antigen specific memory T cells, a process that like the other forms of sensitization takes several weeks. On a subsequent exposure these memory T respond promoting inflammation at the site of exposure. However because the memory T cell response (which requires recruitment and expansion) is slightly slower than antibody mediated memory there is often a delay between exposure and response, with peak responses often seen 2-3 days after inflammation
