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29 Cards in this Set

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what do all helper T cells do

secrete cytokines to turn on other cells

what do all cytotoxic T cells do

kill pathogen infected target cells

how do mature naive T cells become activated

they are activated in the secondary lymph tissue by myeloid dendritic cells (NOT B CELLS OR MACROPHAGES EVEN THOUGH THESE ARE PROFESSIONAL APCs- in fact effector T cells activate them)

the different forms of DCs

called immature DCs in the peripheral tissues; in the lymph nodes they are called mature DCs ro activated DCs; maturation= finger projections

what do macrophages do in the lymph nodes

remove pathogens and their products form the afferent lymph so it prevents infection in the lymph node (VERY important) and its spreading in the blood; also eats any apoptotic lymphocytes

I get the CD4 because it is recognizing things that they process but how do they deal with viral infectious agents? wouldn't the DCs die before they could do their job?

they can; they can also be just a little sick and make it or die on the way and then the viral agent would invade other DCs in the lymph node who quickly present to T cells; or they can try cross presentation from other infected cells (maybe the viral can't infect DCs)

what receptors you DCs have on their surface (besides MHCs?)

all the TLRs except TLR9, and all these increase the efficiency of antigen processing; CCR7 which binds to CCL21 to pull them into the lymph node (where have we seen this before? node also pulls B cells into the node with this set up; DCs also release CCL19 which uses the CCR7 on B cells to pull them to the node)

why do mature naive T cells circulate in the blood if they are not able to recognize antigen there?

they need to travel to all of the nodes because antigen will only be concentrated in one (to begin with) and there are a lot of nodes

homing

the process by which naive T cells leave the bloodstream and enter the T cell zone of a lymph node (similar to the process of neutrophil homing to sites of infection)

how does the T cell enter the lymph node from the blood stream

at the high endothelial venule the LFA-1 on the T cell binds to the ICAM-1on th endothelial cells and the L-selection on the T cell binds to GlyCAM-1 and CD34 on the endothelial cells; the chemokines then pull the T cell through the endothelial wall; L-selectin is replaced by VLA-4 on effector T cells (binds to VCAM-1 on endothelial cells near infection sites) so that they can move through these walls but not be drawn back to the lymph nodes

a conjugate or a cognate pair

DC + T cell (when a connection is realized); the DC then tells the T cell to proliferate and differentiate to form a clone of effector cells all around the star shaped DC

the S1P gradient

pulls effector T cells and mature naive T cells that haven't found their antigen out of the lymph node in the efferent lymph; these T cells express the S1P receptor

CD69

if a T cell finds its antigen in a lymph node it expresses this which causes the S1P receptor to be sequestered so that the cell isn't pulled out of the lymph node

co-stimulatory signal

MHC:peptide:TCR:CD4or8 (maybe called signal 1) is not enough to get the T cell to survive, divide, and differentiate; need T cell CD28 to bind to the DC B7 molecule; maybe called signal 2; anergy without it because no IL-2 made(this ensures that self antigen recognized outside the lymph nodes doesn't produce a response)

SMAC

the region where the DC and the T cell are touching and communicating

ZAP-70

crucial in T cells in order to get them to become effector cells

IL-2

cytokine in the T cell that needs to be turned on in order to made an effector T cell form a mature naive T cell; it works in an autocrine manner; cyclosporin A, tacrolimus, and rapamycin are given to transplant pts to inhibit IL-2 function and this prevents an adaptive immune response

what are the names of the different helper T cells

TH1, TH17, TH2, T follicular helper cells (TFH), and regulatory T cells (Treg)

TH1 cells= what do they do, how do they do it, what transcription factor creates them, what cytokines stimulate their production

activate macrophages, are a major defense against intracellular viral and bacterial infections, cell mediated immunity (TH1 and CD8 are the CMI cells), production of IFN-gamma --> stimulate production of IgG isotypes that facilitate opsonization, phagocytosis, and complement activation, amplify CTL reponse, activate NK cells; they secrete IFN-gamma which binds to the macrophage and CD40 ligand which binds to the CD40 receptor on the macrophage; they only do this when the recognize antigen presented by the macrophage; T-bet; IL-12 from macrophages and DCs and TNFgamma from NK cells; if you use this against TB you get tb leprosy (mild leprosy)

TH17 cells= what do they do, what transcription factor creates them, what cytokines stimulate their production

secrete IL-17 to enhance neutrophil response; RORgammaT; TGF-beta

TH2 cells= what do they do, what transcription factor creates them, what cytokines stimulate their production

activate cellular and antibody response to parasites (eosinophils, basophils, mast cells, and B cells), humoral immunity; inhibit the activation of macrophages (act as a counter measure to TH1 cells); GATA3; IL-4 and IL-5; if you use this against tb you get lepromatous leprosy (bad form)

TFH cells= what so they do, what transcription factor creates them, what cytokines stimulate their production

activate B cells so maturation of the antibody response; in order to do this they need to be further stimulated by their ICOS (inducible T cell co stimulator) receptor binding to the DC ICOS ligand; Bcl6 which is required for the TFH cells to express CXCR5 which is the receptor for the CXCL13 chemokine produced by the stomal cells of the B cell follicle (gets them to interact with the B cells; IL-6

Tregs= what do they do, what transcription factor creates them

suppress other effector T cells; they have CD25 on their surface; they produce TGF-beta and IL-10 which inhibit inflammation and the immune response; FoxP3

cell mediated immunity

a polarized TH1 response dominated by the effector cells of the immune response; characterizes tb leprosy (can get at the leprosy inside the macrophages but can't get them all so the disease moves slowly)

humoral immunity

a polarized TH2 response in which antibodies dominate; characterizes lepromatous leprosy (can't get at the leprosy inside the macrophages)

what's weird about activating a CD8 T cell

it can just be activated by the MHC type I+TCR+CD8 and CD28+B7 but sometimes it needs more to be activated (don't want to accidentally kill a whole bunch of cells) so need a virus specific CD4 T cell to bind to and make MHC type II+TCR+CD4 and CD28+B7 to increase the IL-2 release to super high levels to activate the CD8 T cell; all of this with an infected DC

once it's activated though

once it goes from being naive to being an effector it no longer needs the help of the co-stimulation; the big thing with the co stimulation is to make sure the change from naive to effector occurs in the secondary lymph tissue (see the same thing with CD4 that need to have this change in the presence of DCs) but we want to relax the recognition out in the tissues once they are effectors so that they can do their job

JAK STAT

the binding of cytokines to cytokine receptors activates JAKs which activate STATs which change the pattern of gene expression (phosphorylation pathway that can be undone with phosphatases)

the cytotoxins of CD8 T cells

perforin, granulysin, and serglycin