Immunology Introduction

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LPS: lipopolysaccharide (component of bacteria) which binds to CD14 and interacts with TLR-4
CD14: LPS binds to CD14 on a phagocyte to initiate action of TLR-4
TLR-4: interacts with LPS,CD14 complex to translocate NFkB to nucleus. It is found on phagocytic cells, including Langerhan's cells.
Langerhan's cells: immature dendritic cells that bind and transport skin-derived antigens to lymph nodes where they become activated dendritic cells that can activate lymphocytes. This is an example of a link between adaptive and innate immune system.
IL-6: made by monocytes that were activated by bacterial components to stimulate liver to make factors that bind bacteria including C-reactive proteins.
c-reactive proteins: made by liver after activation of IL-6. It binds to bacterial surfaces acting as an opsonin and also activating complement.
TNF-alpha: Can be secreted by monocytes responding to bacterial infection. Too much TNF-alpha can cause shock as too much fluid is lost from capillaries (non-localized spread of TNF-a) 1) activates local epithelium 2) increases vascular permeability 3) increases IgG and complement entry 4) results in local inflammation, but too much will lead to shock
E-selectin: initiates leukocyte-endothelial interaction by binding Sialyl-Lewis x ligand. It is expressed on endothelial cells.
Sialyl-Lewis x: It is expressed on a leukocyte. There is a weak adhesion between it and E-selectin so the leukocyte rolls along the wall of the bv.
ICAM-1: expressed by endothelial cells and recruits leukocytes expressing Mac-1. This interaction mediates entry of rollling cell into interstitial tissue.
CD4 T cells: "quarterback" of the immune system. Either activates macrophage (TH1) to kill antigen or activates B cells (TH2) to make antibodies
CD8 T cells: Kills infected cells. It can be activated independently of helper T cells by binding to APC directly or being activated by cytokines.
MHC I: "New York" It only binds 8-11 aa peptides and must fit perfectly. It is expressed on most cells. It only presents endogenous peptides. attaches to CD8. Contains 3 alpha chains and beta2-microglobulin. It binds peptide tightly. Proteins cleaved by proteosomes.
MHC II: "California" Binds larger peptides(13-17 aa) and is only found on certain cells. it only presents exogenous peptides. Peptide is bound more loosely. It also binds to CD4. it has one alpha chain and another beta chain (more flexible binding).
B cells: APC function. can recognize "naked" antigen, including carbohydrates (and thus can be activated w/o T cell on occasion). Requires help from T-cell to be activated into plasma cells-->antibodies. B cell is only APC after it has become "experienced"
TCR: T-cell receptor has alpha and beta chain. It undergoes gene rearrangement to diversify. TCR has a weak interaction with antigen so require CD4 and CD8 as well as costimulation to bind tighter
Macrophage: "sentinel" cell. It is activated by T-cells to phagocytose toxins. It also has APC function. They cannot travel. They are also there to restimulate "experienced" T cells (like refueling stations)
Dendritic Cells: relay messages from battle front. It has APC function and unlike macrophages can travel to lymph nodes to activate lymphocytes. They take snapshots of the battle being waged at infected site. They express TLR
Natural Killer Cells: makes sure all cells make MHC1 (except for RBC's) since pathogens will try to escape detection. If a cell does not express MHC1, NK cells will kill it.
M cells: helps transport antigen from gut to underlying tissue
Classical Pathway of Complement System: requires antigen antibody complexes
MB-Lectin Pathway of Complement System: Lectin binds to pathogen surfaces. This is a "smart" bomb.
Alternative Pathway of Complement System: "always on" C3 is spontaneously cleaved. It is like grenades constantly going off.
C1q: binds to antibody or directly to pathogen (usually binds to Ag-Ab complex). It along with C1r and C1s make the C1 complx. once bound, c1r (protease) activated
C2 and C4: both C2 and C4 are cleaved by C1s to make C4b2a = C3 convertase
IgM: most powerful activator of complement (classical) system because of its pentameric structures. default Ig (before class switching to others)
Mannose Binding Lectin: MBL binds to Masp and then when MBL grabs the surface of apathogen MaSP acts like a convertase to clip C3 into C3b. It cannot bind to normal cells surfaces which have sialycic acid
C3-->3a and 3b: cleaved into C3a and C3b. In alternate pathway C3 binds to and is stabilized by B on the surface of pathogen. Then D comes along an clips part of B to make C3bBb. C3 deficiency--bacterial infections.
C3bBb: "chain saw" that cuts other C3. It can also cut of C5 to make C5b
C5b,C6, C7, C8, and C9: Make MAC (membrane attack complex). C9 deficiency-asymptomatic since cells can still lyse w/o 9.
DAF: decay accelerating factor: accelerates destruction of C3bBb convertase. They kick of Bb. It is found on the surface of human cells.
CD59: can kick of MAC's before they form a hole in our cells. It alters last step of attaching C9 to complex. Microbial cells do not have CD59. CD59 deficiency- leads to hemoglobinuria.
C4b and C3b: bind to pathogen surfaces so protein is localized and doesn't go anywhere else. This is done through thioester linkage.
C3a, C4a, and C5a: make capillaries leaky can result in anaphylatoxins
C1 INH: C1 inhibitor dissociates C1r and C1s from C1 complex. deficiency in C1 INH--> hereditary angioneurotic edema
C4b2a3b: also helps cleave C5 but through classical pathway
Factor H: removes Bb from alternative C3 convertase
Factor I: C3B inactivation. deficiency- complement depletion and secondary bacterial infections
CR1: binds C4b displacing C2a or C3b displacing Bb; cofactor for Factor I
properdin-Factor P: complexes with C3b to stabilize C3bBb
TAP I: transports peptides into ER for binding to MHC I molecule
invariant chain: binds to cleft of MHC II while MHC II is in ER of cell so it blocks binding of normal peptides and misfolded proteins.
CLIP peptide: invariant chain after it's been cleaved so a fragment remains in MHC II
tetramers: soluble MHC molecules used to quantify antigen specific T cells
superantigens: recognized by T cells w/o being processed into peptides captured by MHC molecules. It must remain intact to be active so intact molecule is presented by MHC. Example: Toxic shock syndrome
mixed leukocyte reaction (MLR): mixed leukocyte reaction: T cells from one individual are mixed with MHCII carrying cells of another individual to see how they react. It is used to determine histocompatibility
affinity: the ability of one Fab to bind to a single antigen
avidity: stregth by which the whole IgG, IgM, or IgA can bind a polyvalent antigen
RAG: enzymes needed for VDJ rearrangement in B cells RAG also needed in TCR rearrangments
AID: deaminates cystidine to become uridine. only acts on ss RNA. It introduces mutations necessary for somatic hypermutation and class switching. AID is only expressed after activation of B cells
somatic hypermutation: occurs in V joined regions and is initiated by AID after B-cell activation. Point mutations accumulate allowing B cells to have greater affinity for antigen.
class switching: Effects constant regions of immunoglobin. It also requires AID
Fc receptor: bind constant portion of antibodies. They can be found on macrophages. they can also bind complement. Fc can deliver ab to places that can't be reached w/o active transport
CD40/ CD40L: CD40 Ligand expressed by TH2 cell binds to CD40 on B cell. This interaction is needed for class switching, activating B cells, and also needed to allow B cell to survive in germinal centers. This is also needed for T cells to activate macrophages
beta 2-microglobulin: found on all MHC molecules. (same for everyone)
IgG: can diffuse into all tissues. It can activate complement and also opsonize pathogens. It can also help Natural Killer cells in antibody dependent cellular cytoxicity. It can cross placental barrier from mom.
IgE: binds to mast cells and causes them to degranulate--> can cause anaphyltic shock. However, Ige good at defending against parasites.
IgA: protects mucosal surfaces, secreted in milk, resistant to stomach acid Poly-Ig receptor on epithelial cell mediates trancytosis and secretion of IgA
sterile transcripts: Different cytokines signal transcription of various C-regions to make sterile transcripts. This opens up the couble stranded region so AID can come in and make nicks in both strands. Repair machinery comes in and joins switch regions so the selected constant region is near VDJ region.
anchor motifs: found on MHC molecules which bind certain peptides
poly-ig receptor: transcytosis of IgA into secretions into lumen
FcRy: y (gamma) chain used for signally for this FC receptor. Can be found on phagocytic surface. It binds IgG
FcRe: FC receptor binds IgE
ITIM: inhibitory motif on FC receptor
ITAM: activation motif on FC receptor. It is also found on TCR and CD3 molecules (gets phosphorylated by Lck)
J-chain: protein component of IgA and IgM, may be required for polymerization (increases avidity)
CD3: e,y, and & chains. Presented as e& or ye dimers. Required for T-cell receptor signaling. TCR is unique for each cell but CD3 stays the same.
signal pathway for T cell: include lck, IP3, PIP2: 1) antigen binds 2) phosphorylation of ITAM's by lck(found on CD4 or CD8) 3) ITAM's bind Zap70 4)Zap70 phosphorylates lat and SLP76 5) phospholipase C recruited 6) PLC breaks PIP-2 into IP3 and DAG 3)
IP3: opens Ca channels (after being cleaved from PIP2)
DAG: activates protein kinase c--> NFkB or activates Ras--> Fos and AP1 txn (after cleaved from PIP2)
calmodulin: binds ca as part of 2nd messenger system
calcineurin: a serine phosphatase (Ca/Calmodulin-activated) binds to calmodulin and dephsphorylates NFAT to allow it to enter the nucleus to activate gene txn
CD45: tyrosine phosphatase that dephosphorylates and activates Src kinases, Fyn and lck
Ras: small GTPase (small G protein). It exists in two states (1) bound to GTP (active) (2) bound to GDP. Ras activates map kinase kinase pathway ultimately leading to Fos gene transcription or alternatively Fos Jun transcription ( AP-1)
GEF: guanine nucleotide exchange factor: exchanges GDP to GTP
IkB: phosphorylation of IkB relases NFkB enabling it to go to nucleus
AP-1: txn factor (made up of fos une dimer). It induces txn of IL-2
NFAT: activated indirectly by ca release and is released from cytosol by calcineurin. It is also a txn factor that transcribes IL-2. Depending on the type of NFAT produced, either TH1 or TH2 response is made.
NF-kB: activated by protein kinase C which allows NFkB to be released fro IkB sequestration. NFkB is a txn factor impt for IL-2 transcription
NEMO: activated IkB kinase complex that allows NFkB to be released by phosphorylating IkB. Absence of NEMO prevents translocation of NFkB and thus affects B cell CD40 signalling (no class switching) also Toll-like receptor signalling impaired so less macrophage activation. Also conical teeth present.
JAK: tyrosine kinases- part of cytokine pathway that cross phosphorylate each other. they then phosphorylate other associate receptor. This recruits SH2 txn factors known as STATs which dimerize. JAK/STAT is part of cytokine receptor signal transduction.
receptor editing: B-cells get a 2nd or 3rd chance at eliminating self-reactivity by exchanging a new L chain rearrangement for a new one.
allelic exclusion: B cell in bone marrow inherits 2 alleles (from mom and dad) for variable region of heavy chain. If successful rearrangement of this heavy chain occurs on one chromosome, other chromosome is not rearranged. If unsuccessful, then other chromosome is rearrangmed. It can occur at both heavy chain and light chain loci.
surrogate light chain: after VDJ joining of heavy chain, in order to know heavy chain rearrangment is correct. it sends heavy chain out to cell surface with a surrogate light chain to deliver a signal to the cell to say it's ready to move onto light chain rearrangement.
FLT3: expressed on multipotent progenitor cells. Signalling through FLT3 is needed to get to common lymphoid progenitor stage (B,T cells). Lymphocyt differentiation is accompanied by presence of IL-7 receptor.
IL-7: needed for B cell differentiation. It is also needed in order for long lived memory cells to survive
X-linked agammaglobulinemia: genetic defect in B cell formation resulting in low Ig levels. Caused by defect in Btk gene. Susceptible to pyogenic bacteria-pus forming bacteria. They need gamma globulin therapy. You might see absence of tonsils
AIRE: txn regulator that turns on genes in thymus that are not normally expressed. This results in tissue specific proteins being made in thymus to prevent autoimmunity.
FoxP3: important factor for T cells to become regulatory T cells
IPEX: disease resulting from FOXP3 deficiency. It results in decreased function of CD4 CD25 regulatory T cells
Btk (Bruton's tyrosine kinase): essential for B-cell differentiation. a mutation in this gene causes X-linked agammaglobulinemia
zeta chain: Found on TCR and may influence T-cell development
TH1 CD4 cell: activates infected macrophages, especially microbes that persist in macrophages like Listeria and mycobacteria as well as extracellular bacteria). It produces IL-2 and IFN-y. IL-12 also stimulates cells to become TH-1. Usually, TH1 cells are activated by macrophages.
TH2 CD4 cell: gives help to B cells to make antibodies especially switching to IgE. It combats parasites. Usually has a B-cell as its APC. it secretes IL-4,10,5
TH17 T cells: enhance neutrophil response. Good at attacking extracellular bacteria
T regulatory cell: suppress T cell response
L-Selectin: unlike E-selectin and P-selectin, L-selectin is expressed on leukocyte surfaces rather than endothelium. L-Selectin will bind Sialyl-Lewis x of adressins such as CD34, MAdCAM-1, and GlyCAM-1
CD34: vascular addressin that tells the T cell to get out and enter HEV or mucosal tissue. It binds to L-selectin
VLA-4: VLA(very late antigen)-impt for directing effector T cells to inflamed tissues. VLA-4 is an integrin expressed on T cell. It binds to VCAM-1 expressed (on epithelial cell)after T-cell activation so it is impt for targeting these cells to infection sites.
VCAM-1: expresssed on activated endothelium and is impt for recruiting effector T cells
MadCAM: expressed on mucosal endothelium
B7 and CD28: T-cell expresses CD23 and binds to B7 presented on APC--costimulatory signal this is a survival signal.
CTLA-4: binds to B7 on APC so it gives inhibitory signal to T-cell
CCR7: immature dendritic cells comes from bone marrow and encounter pathogens. TLR signalling induces CCR7 expression which directs migration of DC into lymphoid tissue and helps express more co-stimulatory molecules and MHC molecules. CCR7 is also expressed on central memory t-cells that are not activated as quickly as effector memory cells. These cells remain in lymphoid tissue.
IFN-y: TH1 cells make IFN-y to activate macrophages. It can also inhibit production of TH2 cells
IL-4: made by TH2 cells and encourages IgE production by B cells (switch from IgM to IgE after activation by Ag) also a factor in TH2 differentiation: IL-4 signals via stat6
IL-5: made by Th2 cells and encourages IgA production. It also helps eosinophil maturation (allergies)
IL-2: growth factor that stimulates CTL and NK's to proliferate. Made by Th1 cells
Fas-L/Fas: Fas-L on CTL binds to Fas on target cell. This initiates an apoptosis response
IL-10: made by Th2 cells can inhibit Th1 proliferation
histamine: makes bv leaky and can cause airway restriction
TGF-Beta: on it's own can inhibit differentiation of Th17, Th1, and Th2 cells
Th17 cells: first subset of T cells activated in an infection. Activated in presence of TGF-Beta and IL6 (from DCs) It is suppressed by IL-4 or IFN-y. Secretes IL-17 which recruits neutrophils.
STAT4: transduces signal when IL-12 is bound so important for TH1 development
STAT 6: transduces signal for IL-4 so impt for Th2 cell development
CCR5/3: needed for effector memory t cells (migrate to the tissues) and secrete cytokines after restimulation
IL-8: increases ability of leukocyte integrins such as LFA-1 to adhere to their receptors
CD18: common beta chain of three common integrins found on leukocytes (LFA-2, Mac-1, p150,95). Mutation in Cd18 causes leukocyte adhesion deficiency so nerutrophils and monocytes are unable to be recruited to infection site. T cells and B cells can still function normally.
granzymes: serine protease released into a cell to induce apoptosis by cytotoxic t-cell
priming in gut: T-cells are targeted to gut by addressins like MadCam. T cells made in GALT will go to all mucosal places. This is why vaccines are administered through mucosal route to protect multiple mucosal sites.
Intraepithelial Lymphocytes (IEL): mostly CD8 T cells uses perforin and granzymes. found in mucosal tissue. They kill infected/stressed epithelial cells.
gp120: protein on HIV virus envelope that allows the virus to attach to CD4
gp41: HIV envelope protein that promotes fusion of virus with T cell after binding to chemokine receptor
p24: a major core protein of HIV virus that is detected in ELISA assays and western blots testing for the presence of HIV
tat: positive regulator of transcription of HIV
rev: allows translocation of unspliced HIV mRNA to cytoplasm
CCR5: HIV receptor. If inhibited can prevent HIV infection
CXCR4: HIV receptor. If inhibited can prevent HIV infection
LTR: long terminal repeats (sticky ends of RNA that allow HIV genome to be inserted into host DNA
TAR: part of LTR region of HIV RNA. Tat binds to this and allows the RNA to be processed properly
MLR (mixed lymphocyte reaction): Done for tissue typing in organ transplants. Mix T cells of donor with MHC molecules of recipient or vice versa.
crossmatch: done in organ transplants to look for preformed antibodies in recipient such as those against blood type of donor
Rapamycin: blocks signal 3 of T cell in hopes of preventing transplant rejection. it blocks response to IL-2
ASCT (autologous stem cell transplant): wipes out original immune system and gives it hematopoietic stem cells (autologous) to rebuild the immune system
X-linked SCID: severe combined immunodeficiency caused by defective maturation of lymphocytes. The IL-2 receptor is missing its gamma chain. This gamma chain affects other cytokine receptors as well thus affecting both b cells and t cells
Adenosine deaminase deficiency: severe combined immunodeficiency. W/o ADA you have a build up of adensoine-->build up of deoxyATP(toxic). It results in not enough dNTP's to build DNA for B cells and T cells. There are also problems in DNA repairs
severe combined immunodeficiency (Jak/Stat defect): Jak 3 is used by y chain to transduce signal, thus they have the same phenotype as y chain deficiency
DiGeorge Syndrome: decreased IgG (IgG decreases bc no TH2 cell present to secrete cytokins for class switching), seisures and hypocalcemia since they are missing parathyroid gland. they also have no thymus so decreased t cells but normal b cells. Must give them irradiated blood cuz donor T-cells can cause GVH disease
Hyper IgM Syndrome: normal T cells and B cells but absence of CD40 ligand or AID cytidine deaminase (no class switching). Thus, susceptible to bacterial infections such as H-influenzae, strep pneumonia, staph aureus and also suseptible to opportunistic infections (since CD40 needed for activating macrophages)
IgG deficiency: present after 6 months old. give them IV gammaglobulin
IgA deficiency: most common, have sinopulmonary infections, allergic due to failed isotype switch normal B,T cells cannot give blood with IgA bc will have anaphylactic response
Bare Lymphocyte syndrome: IgG deficiency. Mutatiion in MHCII promoter so CD4 cells can't mature so bone marrow transplant needed
Job's syndrome (hyper IgE syndrome): decreased phagocytic chemotaxis so have increased staph, strep, candida. It is the result of STAT 3 mutation. Phagocyte can't be brought to site of infection.
Chronic Granulomatous disease: ineffective phagocytosis. Normal to increased IgG. Causes hot abcesses
antigenic variation: used by pneumoccous pneumonia and influenza virus to avoid recognition
antigenic drift: point mutation on surface molecules of a pathogen prevent it from being recognized
antigenic shift: exchanges of RNA to make new antigenic type (can even occur between 2 species like in swine flu)
trypanosomes: cause sleeping sickness have pre-programmed genetic variation to keep one step ahead of immune system
Latency: Herpes virus and Epstein Bar virus (infects B cells)
Listeria and Mycobacterium tuberculosis: escape killing by escaping contents of lysosomes
treponemes (syphilis and lyme disease) escape mechanism: both coat themselves with host protein
Respiratory Syncytial virus (RSV): early vaccine resulted in enhanced infection (no antibodies were made) Th2 cells release Il3,4,5 which cause bronhospasm
tumor rejection antigens: self antigens recognized as foreign; these are candidate antigens for tumor vaccines. Can be made through point mutations, reactivation of antigen not normally expressed, or overexpression of normal antigen
tumors escape detection by several mechanisms: 1)no costimulation-->anergy of T cell 2)no MHC presentation 3)swallows up ab 4)produces TGF-B
attenuated pathogens: doesn't cause infection
conjugate vaccines: encapsulated bacteria (pneumococcus, meningococcus, etc). Chemical conjugation of polysaccharide and protein
adjuvant for virus: increases it's immunogenicity like adding aluminum salts, small microbial molecules, cytokines, or activating TLR
reverse immunogenetics: can be used to find protective T cell epitopes against a pathogen. you start out with receptor and figure out which proteins it will bind
ISCOM: lipid carriers that induce a powerful ab response-potential way to deliver peptides for vaccine
molecular mimicry: results in autoimmunity when sequences of foreign peptides are similar enough to self peptides to cross react with B and T cells
bystander activation (autoimmunity): -Infected APC produces costimulatory molecule, but then it also expresses on its MHC normal peptides (in addition to pathogenic peptide). This can activate an otherwise anergic T cell in the local area; autoimmunity
"cryptic" self-autoimmunity: some self antigens are sequestered (eye, testis, brain, fetus) However, if presented to APC's can result in destructive autoimmunity
BAFF (autoimmunity): TNf superfamily-inhibiting Baff prevents self reacting antibodies from being made
Anti-BLyS therapy (autoimmunity): binds to B cell survival factors thus killing B cells
rheumatoid arthritis: damages multiple synovial joints in the body. TNF-a and IL-1 (both pro-inflammatory cytokines) suppression has been used as a therapy
LT (lymphotoxin): also known as TNF-beta. It is secreted by killer T-cells in order to destroy infected target cells. It must also be downregulated along with TNF-alpha in order to treat rheumatoid arthritis
IL-1: a proinflammatory factor (involved in fever). It is involved in rheumatoid arthritis pathogenesis
IL-23: involved in inflammation, helps stimulate Th17 cell production,upregulates metalloproteases, and increases angiogenesis
leukotrienes: immune molecules that contribute to inflammation in asthma and bronchitis (100x more powerful than histamine, released by mast cell in later phase)
RAST: used to determine what substances a person is allergic to by measuring IgE levels. They see how many of patients antibodies can crosslink to a given antigen
PAF: platelet activating factor; involved in platelet aggregation, anaphylaxis, and inflammation. It is produced in response to neutrophil, basophil, etc secretions
extracellular bacteria: includes encapsulated bacteria: pneumococcus, haemophilus influenza, staph aureus, streptoccocus response: humoral --> complement activation, associated with C3 deficiency, need TH2 response
opportunistic infection: candida, pneumocystic pneumonia, get this if you have no TH1 or TH2. Also if you have SCID
N gonorrhea, meningococcus: MAC deficiency
intracellular bacteria: mycobacterium leprae and tuberculosis --need cell-mediated response to activate macrophages
removal of spleen: increases susceptibility to bacteria especially encapsulated bacteria such as Streptoccocus pneumoniae H. influenzae
hereditary angioneurotic edema: deficiency in C1INH, swelling of skin and intestine resulting in severe abdominal pain. Decreased levels of C4
Factor I deficiency: C3 rapidly depleted so defective opsonization of bacteria such as staph aureus, h. influenza
C8 deficiency: increased susceptibility to neisserial infections such as meningitis
Graft versus Host Disease: T cells from donor start to attack host cells . It starts with a bright red rash that spreads. It requires taking immunosupressive drugs or anti-T cell antibodies in some instances
Type I hypersensitivity: immediate reaction that is mediated by IgE. It results in mast cells and basophils degranulating. An example of this is allergic rhinitis, anaphylaxis
Type II hypersensitivity: IgG or IgM production that results in activating complement thru IgM or introducing phagocytic destruction via FcyR. An example of this is during blood transfusions that are incompatible or through drugs inducing hemolytic anemia (penicillin) difference btw this and type iii is that antigen is cell-surface bound (not soluble)
Type III hypersensitivity: large amounts of antibodies made that bind to antigen making immune complexes. Complexes are deposited on tissue causing damage. It also causes cell activation when complexes bind to FcyR and also activates complementDrug induced serum sickness is an example (like with penicillin)
Type IV hypersensitivity: delayed hypersensitivity. e.g. PPD test 24-48hrs after exposure. Antigen specific T-lympocytes made which recruit macrophages and cause inflammation which damage surrounding tissue. Example: celiac disease, poison ivy
serum sickness: Type III hypersensitive reaction to animal serum (such as that found in anti-snake venom) Delayed reaction as body produces antibodies to serum. It can also happen with penicillin
disodium cromoglycate: inhibits release of histamine. Used for allergic asthma
tacrolimus and cyclosporin: calcineurin inhibitors. They can bind to calcinuerin to prevent its activation by calcium and block NFAT activation
cyclosporin: block calcineurin signaling (which block NFAT activation, a TF for IL-2) to suppress T cell activation
tacrolimus: block calcineurin signaling (which block NFAT activation, a TF for IL-2) to suppress T cell activation

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