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123 Cards in this Set
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- Back
- 3rd side (hint)
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What does HIV bind to to enter the cell?
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gp120 in HIV binds to CD4; then chemokine receptors to fuse and enter
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What cells does HIV infect?
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those with CD4: Tcells, macrophages, dendritic cells
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What are the two types of chemokine receptors that beind to HIV and what cells express them?
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X4 - resting T Cells
R5 - activated T and macrophages |
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What does HIV virus set point predict?
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speed of HIV progression
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The 6 steps of HIV infection?
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BERIE B
binding, entry, RNA transcription, Integration of DNA into host genome, expression, Budding of new babies! |
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Levels of what increase and stay elevated during HIV infection?
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CD 8 cell count and HIV-Ab counts
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What is HAART?
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Highly Active Antiretroviral therapy
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Definition of AIDS?
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CD 4 numbers less than 200/mm^3
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What should HIV vaccines focus on?
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Induction of CD 8 responses to HIV; this correlates with primary infection control and knockout models show uncontrolled virus replication
also those models that stimulate CD 8 response reduce the set point. |
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Brutons
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X-linked agammaglobulinemia - NO B Cells and thus Ig
btk defect pyrogenic infections such as strep pneumoniae and h influenzae |
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Hyper-IgM
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Cd 40 ligand defect
High IgM but no other Ig Causes pyrogenic infections |
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Ataxia Teleangiectasia
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Low IgA and low T cell #
phosphainositol 3 kinase homologue (effect unknown, but AR inherited; hetero also show symptoms) neurodegenerative, conjunctiva and sinopulm infections |
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WAS
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Wiskcott Aldrich Syndome - small and low platelet #'s - X-linked disorder
Was protein defect treatment: bone marrow transplant low IgM, high IgE and IgA causes pyrogenic infection |
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DiGeorge's?
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Fish face; no thymus (no T cells!), Deletion of Chromosome 22q11
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MHC Class II deficiency
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MHC Class II promoter gene defect which causes low T cell function
leads to severe viral, fungal, and parasitic infections AKA Bare lymphocyte because there isn't MHC on surface! |
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XSCID
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defect in gamma chain of cytokine receptors so stuff like IL-2 can't properly stim proliferation
results in low B and T cell #'s |
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SCID
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AR that end with low T cell and susceptibility to Pneumonia
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Strep and H. influenzae
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pyrogenic encapsulated bacteria that cause sinopulmonary infections
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physiologic hypogammaglobulinemia
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from 4-6 Mo after birth, IgG levels are low until they produce it themselves cause maternal IgG is disappearing.
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Selective IgA deficiency?
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Most common form of immunodeficiency inherited spectrally
caused by block in synth or releaseof IgA - results in GI and sinopulm infections |
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Selective IgM deficiency?
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inability for IgM bearing cells to mature into plasma cells so low IgM in serun
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Neutropenia?
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depletion or dysfunction of neutrophil counts less than 1000/mm^3
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high risk for bacterial infection, result from antineutrophil Ab or secondary to leukemia
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Chediak-Higashi?
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Albinism, chemotaxis defect, granule release defect:
Lazy asian Leukocytes where chemotaxis is messed up. Also abnormal release of lysosomal enzymes. |
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Things that cause defective opsonization?
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agammaglobulinemia,
C3 deficiency, leukocyte adhesion deficiency, systemic lupus (complement consumption) CLAS |
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most essential enzyme in PMNs
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NADPH Oxidase which makes H2O2
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MPO + H202 + ? = toxic agent
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halide
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Chronic granulomatous disease
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NADPH Oxidase deficiency
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CGD causes recurrent infections with what?
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gram positive bacteria; in gram - bacteria, H2O2 is a metabolic product and thus supplies it for the neutrophil
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negative NBT dye test because no superoxide anion made
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MPO deficiency?
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infections but not as bad as CGD chronic granulomatous disease because spontaneous oxidative intermediates are still formed
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Leukocyte G6P dehydrogenase deficiency?
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failure to make NADPH and thus supply O2 radicals for KILLING, same symptoms as CGD where person is sensitive to gram + bacteria
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Only C complement deficiency which is not Autosomal codominantly inherited?
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properdin which is X-linked
it is a regulator that stabilized C3 and C5 cleaving enzymes |
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CD 55
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ends classical complement
aka decay accelerating factor which dissociates C2 and Bb from bound C3 convertase |
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CD 35
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aka CR1 which is a C3b inactivator
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CD 46
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MCP membrane control protein, cofactor for I cleavage of C3b
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CD 59
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expressed by host cells to prevent lysis by the C5b-9 compex (thus the name C59)
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Defect/deficiency of C1q, C2, C3
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poor OPSONIC ACTIVITY
sensitive to encapsulated bacteria |
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deficiency of C 5, 6, 7, 8, or properdin
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can't lyse Neisseria and you prob will have sepsis ewww thats not proper.
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This disease is accompanied by deficiency of classical pathway components
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lupus - C has a role in clearance of immune complexes
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swollen lip
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uncontrolled C4 and C2
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C1-INH defect, swollen lip aka hereditary angioedema
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Factor I and H deficiency
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hypercatabolism of C3 and same as C3 deficiency:
recurrent pyrogenic bacterial sepsis |
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Complement receptor deficiencies?
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CR3 and 4 are on phagocytes; recurrent bacterial infections result as a deficiency and abnormal wound healing (like in LAD)
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deficiency in C9?
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none, as discovered by dr lindt
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recurrent pneumococcus infection
levated WBC Male onset 5-6 months no B cells |
btk gene defect
Bruton's |
treatment: antibiotics, intravenous IgG, chest physiotherapy
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Low IgG levels
2 mo old |
physiologic hypogammaglobulinemia
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totally norm
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IgG < 200 mg/dl but normal IgM and IgA
normal after 2 years of age |
normally asymptomatic transient hypogammaglobulinemia
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Lymphadenopathy
splenomegaly both sexes onset 15-35 yrs |
Common variable immunodeficiency
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mild T or B function abnomalities treated with intravenous IgG, chest physiotherapy, antibiotics
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Most common form of immunodeficiency
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IgA spectrum disorder due to lack of IgA bearing B cells or release into serum
with no direct treatment |
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IgG subclass deficiency
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should be 65: 23:8 ratio of G1, G2, G3 (around 8:3:1)
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CD 40 ligand deficiency on T cell
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Hyper IgM syndrome - X linked
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Cause of graft vs host disease
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combined T and B cell disorder.
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low adenosine deaminase
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SCID - treat with bovine ADA and gene therapy, usually fatal at 12-24 mo
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no stem cells, T and B cell deficieny
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Severe combined immunodeficiency
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deficient expression of HLA class II or I
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AR form of SCID
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Treatment for DiGeorge's
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thymus transplants or hormones
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pt has endocrinopathy for 10-15 years
T and B cell normal negative DTH skin testing to candida |
chronic mucocutaneous candidias
where somehow immune sys likes everything but candida! make sure patient doesn't have Addison's or something else endocrinologic .. |
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Boy with severe ezcema, thrombocytopenia (lack of platelets), onset at 5-6 months
Elevated IgE and IgA but low IgM |
Wiskott-aldrich syndrome - WASp defect
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Graft vs Host
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when immunocompetent cells accidentally get transferred into immunoincompetent pt and the foreign cells destroy the host
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usually fatal
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Disorders that are IgA deficient
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AtaxiA - TelAngictAsiA
ChroniC muCoCutaneous Candidiasis combined immunideficiency selective IgA deficiency |
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Differences between selective IgA and AtaxiaTelangiectasia
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IgA is completely gone in AT
selective IgA T cells are normal. |
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defective phosphoinositol-3-kinase
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ataxia telangiectasia
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Absence of IgA, low IgM
autosomal recessive inheritance T cell # decreased |
ataxia telangiectasia
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Hypersensitivity type and antigen:
myasthenia gravis |
type II non-cytotoxic
ACh receptors |
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Hypersensitivity type and antigen:
Grave's disease |
Type II non-cytotoxic
not an antigen; IgG mimics the hormone to stimulate the thyroid, causing hyperthyroidism |
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Hypersensitivity type:
hay fever |
Type I
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Ag-IgE on activation of mast cells and basophils
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Hypersensitivity type:
asthma |
Type I
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Hypersensitivity type and antigen:
hemolytic anemia |
Type II cytotoxic
RBC |
Initiated by IgG or IgM binding to cell surface antigens
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Hypersensitivity type and antigen:
thrombocytic purpura |
Type II cytotoxic
platelets |
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Hypersensitivity type and antibody involved:
Contact dermatitis |
Type IV
which are Ab independent so no Ab involved |
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Hypersensitivity type:
Tuberculin tests |
Type Iv, which explains why you have to go back 24 hrs later to check it out
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effector cells of Type IV hypersensitivity reactions
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CD 4 and CD 8
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Only hypersensitivity type which is initiated by IgE
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Type I
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cytokines that regulate IgE synthesis?
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IL-4 and IL- 13 induces class switching to IgE
INF gamma inhibits IL-4 induction of class switching (!L-4 vs INFg battle royale over IgE) |
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cytokines that induce Ab class switching to IgG4
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IL 4 and 13
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Antigen requirement for Type I hypersensitivity reaction
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prior exposure and antigen must be bivalent
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Cuase intense bronchoconstriction in Type I hypersensitivity rxns
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LTC4 and LTD4 from basophil and mast cells
also some PGD2 from mast cells |
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IL-5 is released by what?
during when? to cause what? |
IL-5 is released in the late-phase hypersenstivity reaction by Th2 cells which stimulates eosinophil mediator release
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difference between anaphylaxis and anaphylactoid?
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the latter is mast and basophil stimulation by C3a and C5a,
INDEPENDENT OF IgE |
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inhibits antigen-stimulated histamine release
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Cromolyn; only in lung
(ps i have an inhaler with this) |
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action of anti-histamine
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blocks affects of histamine and LTC4/D4, NOT histamine release
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isoproterenol
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beta adrenergic receptor used to reverse bronchoconstriction
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only treatment for anaphylaxis
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Epinephrine, in my purse
an alpha and beta agonist |
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Prescribed for allergies for its potent anti-inflammatory effects
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corticosteroids
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Edema of superficial dermis
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Urticaria aka hives
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treat with antihistamines and corticosteroids
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swelling of lower dermis and subcutaneous tissues
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angioedema
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treat with antihistamine and corticosteroids
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pathways uninhibited in herediatry angioedema
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complement pathway, bradykinin generation
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treat with aminocaprioc acid and androgens
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episodic angioedema without urticaria
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hereditary angioedema
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treat with aminocaprioc acid and androgens
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autoantibodies against C1-INH
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acquired C1-INH deficiency; low C1 levels in blood
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type of hypersenstivity:
allergic contact dermatitis |
Type IV DTH (requires prior exposure because it is cell mediated)
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erythematous papules
thickened skin chronic eczematoid elevated IgE |
atopic dermatitis - Type I
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treat with antihistamines and corticosteroids
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abnormal systemic immune response to drug or bacteria
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hypersensitivity vasculitis
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Erythematous non-blanching papules, fever, malaise, arthralgias, myalgias
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cutaneous necrotizing venulitis
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IgG autoAb to desmoglein 1
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pemphigus vulgaris
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IgG autoAb to HEmidesmosome
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bulllous pemphigoid
(a bull is a HE) |
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Hypersensitivity type:
pemphigus |
Type II cytotoxic - autoantibodies to cell adhesion molecules
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Pt with superficial vasculitis with IgA deposition and prior upper respiratory infection
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Henoch-Schonlein purpura
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intra-epidermal blistering disease
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pemphigus (you can see splitting of basal layer in epidermis ewww)
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Bullous detachment of epidermis resembling scalding
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Stevens-Johnsons syndrom (toxic epidermal necrolysis) it looks like BURN VICTIM
treatment is supportive or if discontinue drug if drug-induced |
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hypersensitivity type:
hypersensitivity pneumonitis |
Type III and IV
BOTH immune complex dependent and Ab independent this is like coal lung and stuffff |
treatment is corticosteroids
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ABPA
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allergive bronchipulmnonary Aspergillosis -
both immediate and immune complex disease |
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fever, productive cough, blood eosinophilia with elevated IgE
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Allergic bronchopulmonary aspergillosis
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Hypersensitivity type:
allergic bronchipulmonary aspergillosis |
Type I and Type III via IgG and IgE
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Lung fibrosis, hemoptysis, glomerulonephritis and inflammation in 35 year old male
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LUNG + KIDNEY = Goodpastures syndrome where Ab attacks basement membrane
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Hypersensitivity Type:
Goodpasture's |
Type II (the collagen is on cell surface of basement membrane)
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disease asociated with c-ANCA
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Wegener's granulomatosis; c-ANCA antibody targets serine protease 3
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treat with prednisone, cyclophosphamide
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Scandinavian-Puerto Rican, 35 year old male with fever, weight loss, SOB, arthritis, cough
granulomas present in various oragans |
Type IV hypersensitivity - sarcoidosis
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Hypersensitivity type:
Sarcoidosis |
Type IV
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antibody that targets serine protease 3
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c-ANCA which is present in Wegener's granulomatosis
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two autoantibodies found in 5% in normal people
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ANA and RF
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Autoab against:
Rh blood group I |
autoimmune hemolytic anemia
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Autoab against:
platelet integrin |
Intrinsic factor
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Autoab against:
cadherin |
pemphigus
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Autoab against:
basement membrane collagen type IV |
goodpastures
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Autoab against:
platelet integrin |
autoimmune thrombocytopenic purpura
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Two features of type II autoimmune diseases
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1)tissue damage restricted to taht tissue
2) they are type II hypersensitivity reactions (Ag is on a cell surface) |
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acute renal failure in a patient with hemoptysis
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goodpasture's
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Hypersensitivity type:
Hashimoto's thyroiditis |
cell mediated Type IV
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Major characteristic of Type III autoimmune diseases
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1)circulating Ag-Ab complexes
2)hypocomplementemia |
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Type III autoimmune disease caused by equine anti-lymphocyte globulin complexes with ALG
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serum sickness
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hormone that strongly affects human SLE
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estrogen (estrogen descreases likelyhood of getting it)
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11 criteria for LUPUS
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SOAP BRAIN MD; 4 or more of these
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high ANA
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lupus
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deposition of Ig-complement at dermal epi-dermal junction
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lupus (in lupus band test)
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Two types of Type IV autoimmune diseases
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Type I DM
hashimoto's thyroiditis |
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