Busy. Please wait.

Forgot Password?

Don't have an account?  Sign up 

show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.

By signing up, I agree to StudyStack's Terms of Service and Privacy Policy.

Already a StudyStack user? Log In

Reset Password
Enter the email address associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know (0)
Know (0)
remaining cards (0)
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Path 6 Immuno


epithel barriers block entry of microbes, phagocytic cells (neutrophils and macrophages), dendritic cells, NK cells, and plasma prots (complement sytem). act via inflamm and anti-viral defense (via dendritic and NK cells) Innate Immunity
Mediated by B lymphos and antibods (Igs) protects against extracellular microbes and their toxins Humoral Immunity (adaptive) - IgM and IgD are on the surface and are the antigen binding component of B-cell receptor complex - IgAlpha and IgBeta transduct signals through the antigen receptor
Mediated by T lymphos protects against intracellular microbes Cellular Immunity (adaptive) - AlphaBeta TCR recognizes peptide antigens displayed by MHC on the surface of APCs - CD3 and Zeta prots transduct signals into T cell after TCR has bound antigen
Most important APC for initiating primary T-cell response. located under epithelia (site of entry of microbes/foreign antigens) and in interstitia of all tissues (where antigens may be produced). express TLRs and Mannose receptors. Dendritic cells - Immature = Langerhans cells - Follicular dendritic cells are located in the lymph follicles of the spleen and present antigens to B cells.
phagocytose microbes, process antigens,m present peptide frags to T cells (APCs in T-cell activation). Also, activated/enhanced by T cells to kill ingested microbes. Also, destroy microbes that are opsonized by IgG or C3b Macrophages
endowed w the ability to kill a variety of infected and tumor cells, w/o prior exposure to or activation by them. express CD16 (lyse IgG coated cells) and CD56. Also, secrete IFN-Gamma, which activates macrophages to destroy ingested microbes. NK cells - IL2 and IL15 stimulate proliferation - IL12 activates killing and secretion of IFN-Gamma
Expressed on all nucleated cells and platelets. encoded by HLA-A,B,and C. Consists of Alphas1,2,and 3 and Beta2. Display peptides derived from prots (antigens) located in the CYTOPLASM and usually produced in the cell. Recognized by CD8+ T lymphos Class I MHC molecules
Expressed on cells that present ingested antigens and respond to T-cells (macrophages, B-cells, dendritic cells). encoded by HLA-D. Consists of Alphas1,2 and Betas1,2. Present antigens that are internalized into vesicles and usually from EXTRACELL microbe Class II MHC molecules
Inflamm diseases, including ankylosing spondylitis, are associated w ... HLA-B27
Autoimmune diseases, including autoimmune endocrinopathies, associated w alleles at the ... DR locus - DR3: Chronic active hepatitis, Sjogren synd, Type 1 Diabetes - DR4: Rheumatoid arthritis, Type 1 Diabetes
Th2 and IgE antibods -> mast cell release of histamine -> vasc dilation, edema, smooth muscle contraction, mucus production, inflamm. Ex: Anaphylaxis, allergies, bronchial asthma Immediate (Type I) hypersense
IgG, IgM -> binds to antigen on target cell-> phagocytosis or lysis of target cell. Ex: Autoimmune hemolytic anemia, Goodpasture synd, Myasthenia Gravis, Graves Antibody-mediated (Type II) hypersense
Depot of antigen-antibod complexes -> complement activation -> recruitment of leukocytes by complement -> release of enzymes/toxic molecules. Inflamm, necrotizing vasculitis. Ex: SLE, serum sickness, poststrep glomnephritis Immune complex-mediated (Type III) hypersense
Activated T cells (Th1, Th17, and CTLs)-> release of cytokines (inflamm and macrophage activation) and T cell mediated cytotox. Granuloma formation. Ex: MS, Type 1 Diabetes, RA, IBD (Crohn), TB Cell-mediated (Type IV) - CD4+ = Delayed Type w Th1 -> macrophages and Th17 -> neutrophils (ex poison ivy rxn) - CD4s + IL-12-> Th1 - CD4s + IL-1,6,or 23 + TGF-Beta-> Th17 - CD8+ = Cytotoxicity w perforins and granzymes (ex Type 1 Diabetes)
Gene most frequently implicated in autoimmunity. when dysfunctional -> lack of control of tyrosine kinases -> excess lymphocyte activation PTPN-22
Chronic, remitting/relapsing, often febrile illness w injury to skin, joints, kidney, serosal membranes. black/hispanic young women. malar rash, photosensitive, arthritis, renal probs, seizure/psychosis, hemolytic anemia, ANAs (anti dsDNA/Smith antigen) Systemic Lupus Erythematosus (SLE) - hydralazine, procainamide, penicillamine can induce SLE-like response (antihistone)
nonbacterial verrucous endocarditis w single or multi 1-3mm warty deposits on any heart valve, distinctively on EITHER surface of the leaflets. Libman-Sacks endocarditis
Dry eyes/mouth from immunological destruction of lacrimal and salivary glands. Anti SS-A (Ro) and SS-B (La). 50-60 y/o women. Sjogren synd
Chronic inflamm d/t autoimmunity, widespread damage to small blood vessels, progressive interstitial and perivascular fibrosis in skin and some organs. Diffuse or limited. W limited can have CREST synd. Anti-Scl 70 and anticentromere antibody. Systemic Sclerosis (Scleroderma) - 50-60 y/o black women - CREST = Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangectasia - anti-Scl 70 (against DNA topo I)-> pulm fibrosis and periph vasc disease - anticentromere antibod-> CRE
Kidney rejection w/in mins or hrs after transplant. rapidly becomes cyanotic, mottled, flaccid, and cortex undergoes outright necrosis (d/t infarction) Hyperacute Rejection
Kidney rejection w/in days of transplant in untreated pt or suddenly months-yrs later, after immunosuppression is stopped. - humoral rejection w vasculitis - cellular rejection w interstitial mononuc cell infiltrate Acute Rejection
progressive renal failure w rise in serum creatinine over 4-6 mos. dominated by vasc changes, interstitial fibrosis, tubular atrophy w loss of renal parenchyma Chronic Rejection
Mainstay of immunosuppression. blocks activation of Nuclear Factor of Activated T cells (NFAT), required for transcription of cytokine genes (like IL-2). Cyclosporine
Immuno competent cells transplanted into immuno crippled recipients, and the transplanted cells recognize alloantigens in the host. most commonly w bone marrow transplant. GVH Acute: rash->desquamation, destroy bile ducts->jaundice, mucosal ulcer->dysentery. Chronic: extensive cutaneous injury w destroy skin appendages and fibrosis of dermis, cholestat jaundice, esophageal stricture, involute thymus/deplete lymphos->infx
Failure of B-cell precursors to develop into mature B cells. mutant cytoplasmic Bruton tyrosine kinase (Btk), on long arm of X chromo. males at 6 mos get recurr bac infx of resp tract. B and plasma cells absent, germinal centers underdeveloped, T rxn norm X-Linked (Bruton's) Agammaglobulinemia - Common variable Immunodef affects both sexes equally
European w extremely low serum and secretory IgA, can be familial or acquired w toxoplasmosis, measels, other viral infx. Mucosal defense is weak->resp, GI, GU infx-> recurrent sinopulm infx and diarrhea Isolated IgA Deficiency
Pts make IgM antibods but are deficient in their ability to produce IgG, IgA, and IgE. most are X-linked mutant CD40L (no Ig class switch). Recurrent pyogenic infx and susceptible to Pneumocystis jiroveci Hyper IgM Synd
T cell deficiency d/t failure of 3rd and 4th pharyngeal pouch formation (4th->thymus, parathyroids, ultimobranchial body). Lose T cell-mediated immunity (no thymus), tetany (no parathyroids), and congenital heart/great vessel defects. 22q11 del DiGeorge Synd (Thymic Hypoplasia)
Defects in both humoral and cell-mediated immune responses. Infants w thrush, diaper rash, fail to thrive. Most common form is X linked mut in common Gamma-chain of cytokine receptors. def IL7->lack T cells/impaired antibody synth. def IL15->lack NK cells Severe Combined Immunodeficiency (SCID) - most commoncause of autosomal recessive SCID is def Adenosine Deaminase (ADA)
X-linked recessive w thrombocytopenia, eczema, vulnerable to recurr infx->early death. progressive secondary depletion of T cells in blood and lymphnodes. IgM low, IgG norm, IgA and IgE high. Prone to developing NHL. d/t mutant WASP Wiskott-Aldrich Synd
Most common Complement def -> SLE-like disease C2 (also other early complements like C1s and C4) - def late complements (C5,6,7,8,9) -> no MAC -> susceptibility to recurr Neisseria infx
Most common HIV in US HIV-1 M B
HIV envelope has 2 glycoprots, what are they? and what is the initial step in infx? What are the coreceptors for the recognition site on gp120? Surface gp120 and a transmembrane gp41. Initial step in infx is binding of gp120 envelope glycoprot to CD4 molecules Coreceptors = CCR5 and CXCR4 (homozygous CCR5 defect = AIDS resistance).
Green birefringence with Congo red stain when observed by polarizing microscopy, and Cross Beta-pleated sheet conformation. Amyloid
Systemic disease w AL type prots (from Ig light chains [Bence Jones prots] mainly Lambda, also excreted in urine). Associated w Multiple Myeloma. Primary Amyloidosis
Systemic disease w AA type prots (from SAA). Secondary to inflamm conditions (RA, ankylosing spondylitis, IBD; also Heroin users; and renal cell CA and Hodgkin lymphoma Reactive Systemic Amyloidosis
Deposition of Beta2-microglobulin, w chronic renal fail, can't be filtered -> carpal tunnel synd Hemodialysis-Associated Amyloidosis
Recessive autoinflamm synd w AA type prots and high cytokine IL-1 production. Fever w inflamm of serosal surfaces. Armenians, Sephardics, and Arabics with pyrin gene. Familial Mediterranean Fever
Dominant w deposition of mutant TTR amyloid in periph and autonomic nerves. Familial Amyloidotic Neuropathies
Created by: Jakphooey