Immuno Flashcards
Head and neck lymph drainage
Cervical nodes
Lung lymph drainage
Hilar nodes
Trachea and esophagus lymph drainage
Mediastinal nodes
Upper limb, breast, skin above umbilicus lymph drainage
Axillary nodes
Liver, stomach, spleen, pancreas, upper duodenum lymph drainage
Celiac nodes
Lower duodenum, jejunum, ileum, colon to splenic flexure lymph drainage
Superior mesenteric nodes
Colon from flexure to upper rectum lymph drainage
Inferior mesenteric nodes
Lower rectum to anal canal (above pectinate line), bladder, vagina (middle 1/3), cervix, prostate lymph drainage
Internal iliac nodes
Testes, ovaries, kidneys, uterus lymph drainage
Para-aortic nodes
Anal canal (below pectinate line), skin below umbilicus (except popliteal area), scrotum, vulva lymph drainage
Superficial inguinal nodes
Dosolateral foot, posterior calf lymph drainage
Popliteal nodes
Lymph drainage of right side of body over diaphragm
Right lymphatic duct
Lymph drainage of everything but right side of body above diaphragm
Thoracic duct
Thoracic duct drains into ____________________
Left subclavian and internal jugular vvs.
Spleen is under _____ ribs
9-11
T cells in the ______________ in the _________ pulp of spleen
PALS, white
B cells in _____________ in the ____________ pulp of spleen
Follicles, white
Splenic dysfunction leads to
Less IgM–>less complement activation –> less C3b opsonization–>more susceptible to encapsulated bugs
Thymus is derived from
3rd pharyngeal pouch
Thymoma
Benign neoplasm of thymus, assn w/ MG and sup. vena cava syndrome
Pathogen recognition in innate immunity
TLRs –. recognize PAMPs like LPS, glagellin, nucleic acids
MHC I binds ________ and _____________
TCR and CD8
MHC I structure
1 long alpha chain and b2 microglobulin
MHC I is in
All nucleated cells
MHC I fxn
Present endogenous antigens to CD8+ T cells – loaded into MHC in RER after delivery via TAP
MHC II binds ______ and _______
TCR and CD4
MHC II structure
2 chains – alpha and beta
MHC II is in
ONLY APCs
MHC II fxn
Present exogenous ags to CD4 helper T cells (loaded after release of invariant chain in acidified endosome)
HLA A3 disease
Hemochromatosis
HLA B8 diseases
Addison disease, MG, Graves
HLA B27 diseases
Psoriatic arthritis, Ankylosing spondylitis, IBD-assc arthritis, Reactive arhtritis (PAIR – seronegative arthropathies)
HLA DQ 2 disease
Celiac disease
HLA DQ8 disease
Celicac disease
HLA DR2 diseases
MS, hay fever, SLE, Goodpasture
HLA DR3 diseases
DM 1, SLE, Graves, Hashitmotos, Addison’s
HLA DR 4 diseases
RA, DM 1, Addison’s
HLA DR 5 diseases
Pernicious anemia, Hashimotos
NK Cell activity is enhanced by
IL 2, IL 12, IFN alpha, IFN beta
NK cell activation in ADCC
CD16 on NK binds to Fc region of bound Ig
Positive selection of T cells – location and selected
Thymic cortex – those with TCRs that can bind self-MHC move on
Negative selection of T cells – location and selected
Thymic medulla – TCRs with high self affinity undergo apoptosis
AIRE fxn
Expresses tissue-restricted self ag in thymus to prevent autoimmune rxn – deficiency –> autoimmune polyendocrine syndrome 1
Th1 Cell secretes
IFN gamma (activates macs) and IL 2
Th1 cell activates
Macs and cytotoxic T cells
Th1 differentiation induction
IFN gamma and IL12 (from macs)
Th1 inhibited by
IL4 and IL10 (from Th2)
Th2 secretes
IL 4,5,6,10,13
Th2 recruits
Eosinophils, promotes IgE prdxn by B cells
Th2 differentiation induction
IL2, IL4
Th2 inhibited by
IFN gamma from Th1
Treg CD expression
CD 3, CD 4, CD 25, FoxP3
Treg cytokines
IL10, TGF beta – anti-inflammatory (suppress CD4/8 fxn)
IPEX
X linked def of FoxP3–> autoimmunity; sx: enteropathy, endorinopathy, nail dystrophy, autoimmune derm conditions, diabetes in male infants
Survival signal in T cell activation
B7 on dendritic cell (CD80/86) w/ CD 28 on naive T cell
B cell class switching
CD40 on B cell binds CD40L on Th
VJ is light or heavy chain?
Light
VDJ is light or heavy chain?
Heavy
Naive B cell Igs on surface
IgD and IgM
IgG properties
Main ab in delayed responce, most abundant Ig in serum; fixes complement, crosses placenta (passive immunity), opsonizes bacteria, neutralizes toxins/viruses
IgA properties
Prevents attachment of bacteria/virus to mucous membranes; monomer in circ vs dimer w/ J chain in secretions; crosses epithelial cells via trancytosis; GI tract – protects against gut infxns; most common ab overall – in tears, saliva, mucus, breast milk
IgM properties
Primary response, fixes complement, monomer on a B cell, pentamer when secreted (w/ J chain)
IgE properties
binds mast cells/basophils; cross links when exposed to allergen –> type I hypersens. and release of histamine; immunity to worms by eosinophil act.; lowest conc.
Thymus independent ags
No peptide component (cannot be presented by MHC) – weak immunogenicity
Thymus dependent ags
Protein component –> class switching and immunologic memory due to direct contact w/ B/Th cells
Cytokine that induces acute phase reactants
IL6
CRP
Acute phase opsonin that fixes complement/facilitates phagocytosis
Ferritin
Acute phase protein that binds/sequesters iron to keep it from bacteria
FIbrinogen
Acute phase coag factor that promotes endothelial repair (correlate w/ ESR)
Hepcidin
Acute phase protein that decreases iron absorption (degrades ferroportin) and iron release (from macs) –> anemia of chronic disease
Serum amyloid A
Acute phase protein that when elevated for a long time –> amyloidosis
Albumin
Downregulated by acute phase –> use of amino acids for positive reactants
Transferrin
Downreg by acute phase –> sequester iron in macs
Classic pathway of complement activated by
IgG or IgM
Alternative pathway of complement activated by
micro surface molecules
Lectin pathway of complement activated by
mannose or other sugars on microbes
Complement factor that opsonizes
C3b
Complement factor that causes anaphylaxis
C3a,4a,5a
Complement factor that causes neutrophil chemotaxis
C5a
Complement factor that causes cytolysis
MAC – C5b-C9
Major body opsonins
C3b and IgG (C3b also helps clear immune complexes)
Inhibitors of complement
DAF/CD55 and C1 esterase inhibitor
C3 Deficiency
Recurrent pyogenic sinus/respiratory tract infxns, increased susceptibility to type 3 hypersens. reactions
C5-9 deficiencies
Neisseria infxns
C1 esterase inhibitor deficiency
Hereditary angioedema due to unregulated activation of kallikrein–>bradykinin; low C4; ACE inhibs are CI
CD55 deficiency
DAF deficiency – complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria
IL1 – secreted by, function
Macs; fever, acute inflammation – activated endothelium to express adhesion molecules, induces chemokine secretion to recruit WBCs
IL6 – secreted by, function
Macs; fever and production of acute phase proteins
IL8 – secreted by, function
Macs; neutrophil chemotaxis
IL12 – secreted by, function
Macs; diff. of T cells into Th1, activates NKs
TNFalpha – secreted by, function
Macs; activates endothelium, WBC recruitment, vascular leak, cachexia in malignancy and maintains granulomas in TB
Sepsis mediators
TNF alpha, IL1, IL6
IL2 – secreted by, function
T cells; growth of helpter, cytotoxic, Tregs, and NKs
IL3 – secreted by, function
T cells; growth and diff. of bone marrow stem cells (like GM-CSF)
IFN gamma – secreted by, function
Th1 cells, NKs; response to ag or IL12 from Macs –> stimulates Macs to kill phagocytosed pathogens, inhibs diff of Th2 cells, activates NKs to kill virus infected cells, increases MHC expression and ag presentation by all cells
IL4 – secreted by, function
Th2 cells; diff of T cells into Th2, growth of B cells, class switching
IL5 – secreted by, function
Th2 cells; growth/diff of b cells, class switch to IgA, growth/diff of eos
IL10 – secreted by, function
Th2 cells, Tregs; attenuates inflamm response, decreases expression of MHC II and Th1, inhibits active macs and dendritic cells
Attenuate the immune response
IL10, TGF beta
Chronic Granulomatous Disease
NADPH ox def; Phagocytes can utilize H2O2 made by invading organisms and convert to ROS, but catalase pos species can neutralize their own (Staph a, Aspergillis) –> infxns
Fxn of pyocyanin and bacteria
P aeruginosa–>generates ROS to kill competing microbes
Fxn of lactoferrin
In secretory fluids/neuts –> inhibits microbial growth by chelating iron
IFNalpha/beta – secreted by, function
Glycoproteins made by cells infected with virus –> other uninfected local cells to prime them for viral defense (help degrade viral nucleic acid/protein)
T Cell general proteins
TCR (binds MHC/ag),
CD3 (w/ TCR for transduction of signals),
CD28 (binds B7 on APC for co stim signal),
Th surface proteins
CD4,
CD40L
CXCR4/CCR5 (coreceptors for HIV)
Tc surface proteins
CD8
Treg surface proteins
CD4
CD25
B cell surface proteins
Ig CD19,20,21 (EBV receptor) CD40 MHCII B7 (costim when APC)
Macs surface proteins
CD14 (for PAMPs) CD40 CCR5 MHCII, B7 Fc and C3b receptors for phagocytosis
NK cell surface protein
CD56
Hematopoietic stem cell surface protein
CD34
Superantigen MOA
Released by strep pyo/staph aureus –> cross link beta region on TCR to MHCII on APCs –> massive activation of CD4 T cell–>lots of cytokines
Endotoxin/LPS MOA
Directly stim macs by binding TLR4/CD14 (no T cell involvement)
Salmonella antigenic variation
Flagellar variants
N. gonorrhea antigenic variation
Pilus protein
Toxins where unvaccinated pts should be treated with preformed antibodies
Tetanus, botulinum, HBV, rabies, diptheria (passive immunity) – HBV and rabies give passive and active
Live attenuated vaccine induces _____ immunity
Cellular AND humoral – usually lifelong, but can revert to virulent to CI in preg/immunodef
Examples of live attenuated vaccines
BCG, intranasal flu, measles, mumps, Sabin polio, rotavirus, rubella, varicella, yellow fever
Killed/inactivated vaccines induce ______ immunity
Humoral only – cannot revert but usually a weaker response and requires boosters
Examples of killed/inactivated vaccines
Rabies, flu shot, Salk polio, hep A
Vasoactive amines act at
Postcapillary venules
Type I delayed phase is due to
Mast cells and basophils releasing cytokines
Type II hypersensitivity
Abs bind cell surface ags –> cell drestruction, inflamm, cellular dysfxn
Examples of cellular destruction type II HS
Autoimmune hemolytic anemia, immune thrombocytopenic purpura, transfusion rxns, hemolytic disease of newborn
Examples of inflammation type II HS
Goodpasture syndrome, rheumatic fever, hyperacute transplant rejection
Examples of cellular dysfuction type II HS
Graves disease, MG
Type III HS
Immune complex (IgG complexes activate complement –> recruit neuts –> release lysosomal enzymes
Examples of type III HS
SLE, polyarteritis nodosa, post streg glomerulonephritis (vasculitis, systemic)
Serum sickness
Immune complexes form when abs are made to foreign proteins –> deposit in membranes and fix complement –> most often caused by drugs; sx: fever, urticaria, arthralgia, proteinuria, lymphadenopathy 5-10 days after exposure
Arthus rxn
Intradermal injxn of ag in presensitized individual –> immune complexes in skin –> edema, necrosis, activation of complement
Type IV HS types
Direct cell cytotoxicity: CD8+ T cells kill targeted cells
Delayed-type: sensitized CD4 Ths release cytokines activating macs and inflammation
NO Abs
Examples of type IV rxns
Contact dermatitis, graft vs host disease, PPD, patch test
Allergic/anaphylaxis in blood transfusion sx and time window
Urticaria, pruritis, fever, hypotension, respiratory arrest, shock
mintues to 2-3 hours
Febrile nonhemolytic transfusion rxn – pathogenesis, sx, time window
Type II HS (host abs against donor HLA and WBCs or induced by cytokines that accumulate in storage
Sx: fevers, headaches, chills, flushing
1-6 hrs
Acute hemolytic transfusion rxn – pathogenesis, sx, time window
Type II HS –> intravascular hemolysis (ABO incompatibility) or extravascular hemolysis (host rxn against foreign ag on donor RBCs)
Sx: fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria (intravasc) or jaundice (extravasc)
w/in an hour
TRALI – pathogenesis, sx, time window
Donor anti-leuk abs against recipient neuts and pulmonary endothelium
Sx: respiratory distress, non cardiogeneic pulmonary edema
W/in 6hrs
Anti Achr
MG
Anti-glomerular basement membrane
Goodpasture
Anti-B2 glycoprotein
Antiphospholipid
Anticardiolipin, lupus anticoag
SLE, antiphospholipid syndrome
Anticentromere
CREST
Antidesmoglein/desmosome
Pemphigus vulgaris
Anti-glutamic acid debarboxylase
T1 DM
Islet cell cytoplasmic abs
T1 DM
Antihemidesmosome
Bullous pemphigoid
Anti Jo1/synthetase
Polymyositis dermatomyositis
Anti SRP
Polymyositis, dermatomyositis
Anti helicase/Mi-2
Polymyositis, dermatomyositis
Antimicrosomal
Hashimotos
AntiTG
Hashimoto
AntiTPO
Hashimoto
Antimitochondrial
Primary billiary cirrhosis
Antiparietal cell
Pernicious anemia
Anti IF
Pernicious anemia
AntiPLA2r
Primary membranous neprhopathy
AntiScl70 (DNA topo I)
Diffuse scleroderma
Anti smooth muscle
Autoimmune hepatitis type 1
Anti SSA (Ro) SSB (La)
Sjorgrens
AntiTSHr
Graves
Anti presyn. voltage gated Ca channel
Lambert Eaton myasthenic syndrome
IgA anti endomysial
Celiac
IgA Anti TTG
Celiac
p-ANCA
MPO! Microscopic polyangiitis, eosinophilic granulomatosis w/ polyangiitis (Churg Strauss), ulcerative colitis
c-ANCA
PR3! Granulamatosis w polyangiitis (Wegener)
Rheumatoid factor (IgM against IgG Fc)
RA
Anti-CCP
RA
ANA
SLE (but nonspecific)
Anti-dsDNA
SLE
Anti Smith
SLE
Anti histone
Drug induced lupus
Anti-U1 RNP
Mixed connective tissue disease
Bruton agammaglobulinemia – genetics, sx, findings
X linked defect in BTK (B cell maturation)
Sx: recurrent bacterial and enteroviral infxns after 6 mts
Find: No B cells in peripheral blood, univerally low Ig, scanty lymph nodes/tonsils
NO VACCINES
Select IgA def – genetics, sx, findings
Most common one
Sx: usually assymptomatic, some airway/GI infxn, autoimmune disease, atopy, anaphylaxis to IgA products
Find: low IgA, normal IgG/IgM, lots of giardiasis
CVID – genetics, sx, findings
Defect in B cell diff
Sx: after age 2 –> increased risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmnoary infxn
Find: low plasma cells, low Ig
Thymic apalsia – genetics, sx, findings
Digeorge – 22q11 deletion/failure to develope 3/4th pharyngeal pouch –> no thymus or parathyroids
Sx: Tetany (hypocalcemia), recurrent viral/fungal infxns (low T cells), conotruncal abnormalities (tet of Fallot, truncus arteriosus)
Find: low T cells, low PTH, low Ca, no thymic shadow on CXR
IL12r deficiency – genetics, sx, findings
Ar – less Th1 resposne
Sx: Disseminated mycobacterial/funcal infxns – may present after BCG vax
Find: low IFNgamma
Hyper IgE syndrome – genetics, sx, findings
AD – def of Th17 cells due to STAT3 mutation –> impaired recruitment of neuts (Job syndrome)
Sx: coarse facies, cold staphylococcal abscesses, retained primary teeth, high IgE, derm problems (eczema), bone fractures from minor trauma
Find: high IgE, low IFN gamma, high eos
Chronic mucocutaneous candidiasis – genetics, sx, findings
T cell dysfxn
Sx: Noninvasive candida infxns of skin/mucous membranes
Findings: No t cell prolif in response to candida ags or cutaneous rxn to candida ags
SCID – genetics, sx, findings, tx
IL-2R gamma chain – X linked or ADA deficiency – Ar
Sx: Failure to thrive, chronic diarrhea, thrust, recurrent infxns of all kinds
FInd: Low t cell receptor excision circles, no thymic shadow on CXR, no germinal centers, no T cells by flow cyto
Tx: No live vax, give antibiotic prophylaxis, IVIG, bone marrow transplant curative
Ataxia telangectasia– genetics, sx, findings
Defects in ATM gene –> failure to repair DNA double strand breaks –> cell cycle arrest
Sx: cerebellar defects (ataxia), spider angiomas (telangectasia), IgA def
Find: High AFP, low IgA, IgG, and IgE, lymphopenia, cerebellar atrophy, high risk of lymphoma/leukemia
Hyper IgM– genetics, sx, findings
Usually defective CDL on Th –> class switching defect, is Xr
Sx: Severe pyogenic infxns in early life, opportunistic infxns w/ PCP, cryptosproridum, CMV
Find: Low IgG, IgA, IgE, fails to make germinal centers
Wiskott Aldrich Syndrome – genetics, sx, findings
Mutation in WASp gene – leukocytes and plts cannot reorg actin cytoskeleton to present ags, Xr
Sx: Thrombocytopenia, eczema, recurrent pyogenic infxns, increased risk of autoimmune disease and malignancy
Find: High Ige, IgA, fewer/smaller platelets
Leukocyte adhesion def type 1– genetics, sx, findings
Defect in LFA-1 integring (CD18) on phagocytes – impaired migration/chemotaxis, Ar
Sx: Recurrent skin/mucosal bacterial infxns, absent pus, impaired would healing, delayed separation of umbilical cord (>30d)
Find: Increased neuts but none at sites of infxn
Chediak Higashi – genetics, sx, findings
Defect in LYST – microtubule dysfxn in phagosome/lysosome fusion. Ar
Sx: Recurrent pyogenic infxns by staph and strep, partial albinism, peripheral neuropathy, progressive neurodegen, infiltrative lymphohistiocytosis
Find: Giant granules in granulocytes and plts, pancytopenia, mild coag defects
CGD – genetics, sx, findings
Defect in NADPH oxidase – less ROS and respiratory burst in neuts, usually Xr
Sx: Increased susceptibility to cat pos organisms
Finding: Abnormal dihyrorhodamine (flow cyto – less green fluorescence) and nitroblue tetrazolium does NOT turn blue
T cell def infxns
Viral (CMV, EBV, JCV, VZV, respiratory/GI) and fungal/parasites (candida, PCP, cryptococcus)
B cell def infxns
Encapsulated bacteria (SHINE my SKiS), enteroviral encephalitis, polio, GI giardiasis
Granulocyte def infxns
Staph, Burkholderia cepacia, P. aeruginosa, Serratia, Nocardia, Candida (systemic), Aspergillus, Mucor
Complement def infxns
Early: encapsulated species
Late: Neisseria
Hyper acute transplant rjxn timing, pathogen
Minutes –> preexisting abs react to donor ag (type II) –> complement activation –> thrombosis of graft vessels, ischemia, necrosis –> must remove graft
Acute transplant rjxn timing
Weeks to months
Cellular acute transplant rjxn pathogen
CD8 T cells against donor MHCs (type IV HS rxn)
Humoral acute transplant rjxn pathogen
Similar to hyper acute by abs after transplant
Acute transplant rjxn sx
Vasculitis of graft vessels w/ interstitial lymph infilitrate – prevent/reverse w/ immunosuppressants
Chronic rjxn timing, pathogen, sx
Months to years
CD4 t cells respond to RECIPIENT APCs presenting DONOR peptides – both cellular and humoral (type II and IV HS)
Recipient T cells react and make cytokines –> prolif of vascular smooth m., parenchymal atrophy, interstitial fibrosis, arteriosclerosis
GVHD
Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells w/ foreign proteins –> type IV HS leading to organ failure
Sx: Maculopapular rash, jaundice, diarrhea, hepatosplenomegaly
Bone marrow and liver transplants because lots of lymphs
Can be beneficial in leukemia (graft vs tumor)
Cyclosporin MOA, indications, ADE
MOA: Calcineurin inhibitor (binds cyclophilin) –> blocks T cell activation by preventing IL 2 transcription
Indicated: Psoriasis, RA, transplants
ADE: NEPHROTOXIC, htn, hyperlipidemia, neurotox, gingival hyperplasia, hirsutism
Tacrolimus MOA, indications, ADE
MOA: Calcineurin inhibitor binds FK506 binding protein – blocks T cell activation by preventing IL 2 transcription
Indication: transplants
ADE: NEPHROTOXIC, increased risk of diabetes and neurotox
Sirolimus (rapamycin) MOA, indications, ADE
MOA: mTOR inhibitor – binds FKBP blocking T cell activation and B cell differentiation by preventing a response to IL 2
Indication: kidney transplants
ADE: Pancytopenia, insulin resistance, hyperlipidemia
Basiliximab MOA, indications, ADE
MOA:blocks IL-2r
Indication: Kidney tranplant
ADE: Edema, HTN, tremor
Azathioprine MOA, indications, ADE
MOA: Antimetabolite precursor of 6MP – inhibits lymph prolif by blocking nucleotide synth
Indication: Transplats, RA, Crohn disease, glomerulonephritis, autoimmune conditions
ADE: Pancytopenia, degraded by XO to tox increased by allopurinol in gout tx
Mycophenolate mofetil MOA, indications, ADE
MOA: Reversibly inhibits IMP DH – prevents purine synth of B and T cells
Indication: Transplants, lupus nephritis
ADE: Gi upset, pancytopenia, HTN, hyperglycemia, invasive CMV infxn
Corticosteroids MOA, indications, ADE
Inhibit NF-KB – suppresses B and T cell fxn by decreasing transcription of cytokines, induces T cell apoptosis
Indication: transplants, autoimmune/inflam disorders, adrenal insufficiency, asthma, CLL, non-Hodgkin lymphoma
ADE: Cushing syndrome, osteoporosis, hyperglycemia, diabetes, amenorrhea, adrenocoritcal atrophy, peptic ulcers, psychosis, cataracts, avascular necrosis of femoral head, adrenal insufficiency if stopped abruptly
OTHER: WBCs demarginate – looks like leukocytosis
Use of aldesleukin (IL2)
Renal cell carcinoma, metastatic melanoma
Use of epoetin alfa (EPO)
Anemias (w/ renal failure)
Use of filgrastim (G-CSF)
Recovery of bone marrow and WBC counts by granulocyte stim
Use of Sargramostim (GM-CSF)
Recovery of bone marrow and WBC counts by granulocyte and monocyte stim
Use of IFN alpha
Chronic hep B/C, Kaposi sarcoma, malinant melanoma, hairy cell leukemia, condyloma acuminata, renal cell carcinoma
Use of IFN beta
Multiple sclerosis
Use of IFN gamma
CGD
Use of romplostim (thrombopoetin analog) and eltrombopag (thrombopoietin receptor agonist)
Thrombocytopenia
Use of oprelvekin (IL1)
Thrombocytopenia
Alemtazumab target and use
CD52
CLL, MS
Bevacizumab target and use
VEGF
Colorectal cancer, renal cell carcinoma, non-small cell lung cancer, Neovascular age-related macular degeneration, proliferative diabetic retinopathy, macular edema
Cetuximab target and use
EGFR
Stage IV colorectal cancer, head and neck cancer
Rituximab target and use
CD20
B cell non hodgkin lymphnoma, CLL, RA, ITP
Trastuzumab target and use
HER2/neu
Breast cancer, gastric cancer
TNF alpha inhibitors
Adalimumab, certolizumab, golimumab, infliximab, etanercept (decoy TNF alpha receptor)
TNF alpha inhibitors use
IBD, RA, ankylosing spondylitis, psoriasis
Dacalizumab target and use
CD25 (part of IL2 receptor)
Relapsing MS
Eculizumab target and use
Complement part of C5
Paroxysmal nocturnal hemoglobinuria
Natalizumab target and use
alpha4-integrin (WBC adhesion)
MS, Crohn disease
WARNING: Risk of PML in pts w JCv
Ustekinumab target and use
IL12/IL23
Psoriasis, psoriatic arthritis
Abciximab target and use
Plately glycoproteins IIBIIIA
Antiplt agent for preventing ischemic complications in pts undergoing PCI
Denosumab target and use
RANKL
Osteroporosis, inhibits osteoclast maturation by mimicking osteoprotegrin)
Dig immune Fab target and use
Dig tox
Omalizumab target and use
IgE – prevents IgE binding to FcERI
Refractory allergic asthma
Palivizumab target and use
RSV F protein
RSV prophylaxis for high-risk infants
Ranibizumab target and use
VEGF
Neovascular age-related macular degeneration, proliferative diabetic retinopathy, macular edema
