t cells

Question 1

t cell role in immune sytsem

Answer 1

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.

Question 2

what is Type I hypersensitivity

Answer 2

is an allergic reaction provoked by re-exposure to a specific type of antigen referred to as an allergen

Question 3

what type of antibodies mediate the response

Answer 3

IgE

Question 4

why do non allergic people make IgE

Answer 4

Non-allergic individuals predominantly only make IgE in response to parasitic infections or very potent venoms

Question 5

worst sort of antibodies do

Answer 5

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

Question 6

describe a test used for testing allergies

Answer 6

Skin prick tests. Exposing the skin to small amounts of allergen can often be used to diagnosis allergy.

Question 7

what is the end result of the allergy

Answer 7

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

Question 8

what il act on b cells to produce IgE

Answer 8

il 4

il 13

Question 9

is IgE found in circulation

Answer 9

IgE is very rarely found in the circulation, even in allergic individuals

Question 10

what happens to teh IgE on the im

Answer 10

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.

Question 11

what is the early phase

Answer 11

bioactive small molecules produced directly by mast cells, occurs within minutes of allergen exposure

Question 12

A later response

Answer 12

often seen within a few hours is the result of the recruitment of early inflammatory cells such as neutrophils.

Question 13

A third phase, or late response

Answer 13

is often peaks 3-4 days after exposure where high frequencies of eosinophils are recruited and Th2 cells are present
.

Question 14

Type II hypersensitivity

Answer 14

antibody-mediated cytotoxic hypersensitivity, involves the destruction of cells by IgG or IgM antibody bound to antigens present on the surface of the cells

Question 15

example of type 2 hypersensitivity

Answer 15

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.

Question 16

type 2

Answer 16

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.

Question 17

antibody diseases

Answer 17

Anti-receptor activity – blocking or activating its function
Antibody dependent cell-mediated cytotoxicity (abbreviated to ADCC)
Classical activation of the complement cascade

Question 18

complement cascade is what

Answer 18

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

Question 19

what can the cc result in

Answer 19

inflammation, opsonisation and recruitment and activation of immune cells.

Question 20

the ADCC antibody-antigen complexes on the surface of cells are bound by Fc receptors are found where

Answer 20

expressed by cells such as granulocytes and NK cells

Question 21

result in

Answer 21

inflammatory mediators, chemokines and cytokines.

Question 22

summary result of type 2

Answer 22

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.

Question 23

what is type 3

Answer 23

Type III hypersensitivity is sometimes known as immune complex driven disease

Question 24

immune complexes are what

Answer 24

Immune complexes are non-cell bound antigen-antibody complexes which are normally cleared through the activity of the immune system

Question 25

what can happen of immune complexes are not cleared

Answer 25

the immune complexes end up being deposited in the blood vessel walls and tissues, promoting inflammation and tissue damage

Question 26

results in what

Answer 26

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

Question 27

Type IV hypersensitivity

Answer 27

, other known as delayed-type or T cell mediated hypersensitivity, is primarily initiated by T cell

Question 28

how it works

Answer 28

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