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Flashcards in Cellular cooperation Deck (17)
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1
Q

CD4’s effect on other leukocytes

A
  • acts as T helpoer for b cells to make ig
  • activates cell mediated immunity (cd8, nk, and macrophages)
  • activate effector cells of innate immunity (eosinophils, neutrophils)
2
Q

general mechanism of cd4 activation

A
  • antigens interact with APC,
  • thic complex secretes cytokines
  • cd4 t cell binds to antigen mhc complex
  • cd4 t cell differentiates into subset
  • different effector cells are activated based upon the subset
3
Q

Th1

A
  • involved in response to intracellular pathogen, virus and bacteria
  • secretes IFNgamma and IL2
  • activates cd8, nk, and macrophages
  • activated effector then go do kill cells that are infected with the virus
4
Q

Th2

A
  • involved in the response to wormsm and allergens
  • IL4 is present early on but we do not know where it comes from
  • it stimulates, along with the MHC antigen complex, cd4 t cells to differentiate into Th2
  • Th2 releases IL5, IL4 and IL13
  • IL5 ativates eosinophils
  • IL4 and 13 activate plasma cells which produce IgG4 and IgE
  • IgE and eosiniphils are the effectors of the Th2 response
  • also involved in asthma (high eosinophils and IgE)
5
Q

Th17

A
  • responses to fungi and extracellular bacteria
  • releases IL17
  • this is a proinflammatory response which activates neutrophils and epithelial cells, especially at mucosa surfaces
  • also involved in atuo-inflammatory conditions such as rheumatoid arthritis, multiple sclerosis and psoriasis
6
Q

cross inhibition of subset function

A
  • once a subset is produced, it starts releasing its signature cytokines
  • these cytokines inhibit the production of the other cd4 t cell subsets
7
Q

thymus dependent antigens

A

-require help from cd4 t helper cells in order for b cells to synthesize antibodies

8
Q

Th are required for

A
  • formation of germinal center in LN

- generation of long-lived antibody responses after infection or vaccination

9
Q

interaction of antigen with antigen specific b and t cells in a lymph node

A
  • B cell captures and internalizes antigen via ig
  • b cell presents peptide on MHC class 2 to a cd4 cell
  • dendritic cell bearing the same peptide activates cd4 with the right TCR in the t cell area of the node
  • this
10
Q

Th-B cooperation in antibody sythesis

A
  • mutual activation of the Th and B cell
  • cytokines and cell surface interactions
  • Th synthesizes cytokines and b cells make ab
  • activation requires the first signal of peptide and mhc 2 binding to TCR then the second signal of costimulator pairs B7 and CD28, CD40 and CD40L
11
Q

what do the cytokines made by the t cell after activation by a b cell determine?

A

-the class of ab that the b cell will produce once differentiated

12
Q

CD40 binding to CD40 ligand is important for what?

A

-activation od AID which helps in class switch reombination

13
Q

a defect in class switch recombination results in what and stems from what

A
  • stem from defects in CD40, CD40L, or AID

- this causes hyper IgM syndrome: increased igM, decreases IgG/A/E

14
Q

thymus independetn antigens and Ab response

A
  • do not require t cell help for b cells to secrete ab’s
  • LPS
  • capsular polysaccharide: strep pneumoniae and flu B
  • IgM predominates, no t cell derived cytokines, no class switch
  • no memory, b cells witch make IgM are not memory cells
  • hard to make vaccines (however conjugate vaccines linked to proteins allow us to circumvent)
15
Q

cd8 t cells

A
  • must be activated before they kill their target which is typically a virus infected or tumor cell
  • activation separable from killing phase
  • several mechanisms to activate
  • requires 1st and 2nd signal from APC (usually DC) and cytokines
  • most viruses need cd4 t cells to activate cd8 cells, some do not
16
Q

how does a cd8 kill its target cell?

A
  • interacts with a cell producing its counterpart MHC class 1
  • the cd8 then releases granules from the surface of the cell closest to the cell expressing the mhc
  • these granules(serine esterases) form a pore in that cell and enter in order to activate apoptosis
  • it can also do this through Fas L and Fas R
17
Q

turning off the t cell response

A
  • induction of cell surface molecules that inhibit the reponse
  • this signal is transmitted via the CTLA receptor on the activated t cell
  • expression of PD-1 on proliferating t cells and interaction with PDL-1/2 is also inhibitory, this is called t cell exhaustion