Immunology 1 Flashcards
0
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Adaptive immunity
A
Slower on first exposure, specific. Cell mediated (T) and humoral (B).
1
Q
Innate immunity
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Rapid, nonspecific. E.g. physical barriers, cells (neutrophils, macrophages, dendritic cells), complement.
2
Q
Passive immunity
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Type adaptive immunity. Preformed Abs from source outside body. E.g. milk, antitoxins, Abs (HBV, rabies)
3
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Active immunity
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Type of adaptive immunity.
Body’s intrinsic mechanism to fight infection.
Lymphocytes, lymphoid organs
4
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Primary lymphoid organs
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Bone marrow, thymus.
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Secondary lymphoid organs
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Spleen, LNs.
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Q
Site of positive and negative selection of T cells
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Starts in corticomedullary junction in thymus, continues until reaches medulla.
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Embryology of thymus
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3rd branchial pouch
8
Q
Parenchyma of spleen
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Red pulp and white pulp
9
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White pulp (spleen)
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Immune cell interaction. Central arteriole surrounded by PeriArterial Lymphatic Sheath
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Red pulp (spleen)
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RBC storage and turnover. Rich vasculature with splenic cords and fenestrated capillaries.
11
Q
Marginal zone (spleen)
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Separates red and white pulp.
Contains APCs.
12
Q
Primary lymph nodes
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Inactive follicles.
Stored lymphos awaiting antigen presentation
13
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Secondary lymph nodes
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Active follicles.
Pale germinal centers within cluster lymphos. B cells proliferate here and produce Abs.
14
Q
Lymph drainage-stomach
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Celiac
15
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Lymph drainage-upper arm, lat breast
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Axillary
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Lymph drainage-duodenum, jejunum
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Superior mesenteric
17
Q
Lymph drainage-sigmoid colon
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Colic -> inf. mesenteric
18
Q
Lymph drainage-lower rectum and anal canal above pectinate
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Internal iliac
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Lymph drainage-anal canal below pectinate
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Superficial inguinal
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Q
Lymph drainage-testes
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Para-aortic
21
Q
Lymph drainage-scrotum
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Superficial inguinal
22
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Lymph drainage-superficial thigh
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Superficial inguinal
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Lymph drainage-lat side dorsum foot
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Popliteal
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Cells of innate immunity
Phagocytic cells, APCs, NK cells
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Phagocytes
Neutrophils
Macrophages
Dendritic cells
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Antigen Presenting Cells (APCs)
Dendritic cells
Macrophages
B cells
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NK cells
Contain lytic granules that attack and kill virus infected or tumor cells via antibody-dependent cellular cytotoxicity
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Activation of classic pathway (complement)
C1 recognizes and binds constant fragment of IgG or IgM
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Activation of alternative pathway (complement)
Activated C3 recognizes certain nonspecific antigens
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Activation of lectin pathway (complement)
Mannose-binding lectin recognizes carbohydrate antigens on surfaces of microorganisms
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C1 esterase inhibitor
Breaks apart C1.
| Deficiency leads to hereditary angioedema, due to uncontrolled activation classic pathway
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Decay Accelerating Factor (DAF)
Disrupts formation C3 convertase, thus halts complement.
If protein that associates DAF with RBC abnormal, can result in Paroxysmal Nocturnal Hemoglobinuria, as RBCs are more susceptible to complement-induced hemolysis.
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C5b-C9 deficiency
Recurrent Neisseria infections
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Deficiency in C3a, C3b
Recurrent pyogenic infections (respiratory tract)
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Tc cells
CD8. Kills cells infected with viruses or intracellular bacteria
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Main function of B cells
Recognize extracellular pathogens and differentiate into plasma cells that produce Abs
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Functions of Abs
Opsonization
Neutralization
Complement activation
Antibody-dependent cellular cytotoxicity
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MHCs
Encoded by HLA genes.
| Most important molecules in transplantation
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MHC I
On all nucleated cells
Present intracellular peptides
Binds TCR, CD8+ coreceptor
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MHC II
On APCs
Present extracellular peptides (engulfed antigens)
Binds to TCR, CD4+ coreceptor
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Hyperacute rejection
Preformed antidonor Abs. Minutes.
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Acute rejection
Tc reaction with foreign MHCs. Reversible with immunosuppression, Weeks.
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Chronic rejection
Ab mediated damage of vasculature. Irreversible. Months-years.
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Graft v host disease
Irradiated immunocompromised host. Grafted T cells recognize body as foreign.
Rash, jaundice, diarrhea
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CD3
Mature T cells. Assoc with TCR
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CD4
Th. Coreceptor fo MHC II on APCs.
| Coreceptor for HIV
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CD8
Tc. Coreceptor for MHC I.
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CD40
Isotype switching
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CD28
T cell activation
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CD19, CD20
B lymphocytes
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CD21
Complement pathway, EBV receptor
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IFN-alpha, IFN-beta
Signal cell to produce protein to decrease viral mRNA
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IFN-gamma
Increases expression MHC I and II; stimulates phagocytosis by macrophages.
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T cell activation
TCR binds antigen on MHC of APC, then costimulatory molecule required.
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Isotype switching
Naive B cells express IgM but do not secrete Ab until activation and isotype switching occurs.
When IgM binds antigen, antigen peptides loaded onto MHC II. When that MHC II binds to TCR, CD4 + CD40, T cell produces cytokines which induce isotype switching
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T cell anergy/tolerance-mechanisms
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Positive selection (thymic cortex)
Negative selection (thymic medulla)
Peripheral tolerance by clonal deletion, anergy, active suppression, ignorance.
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Positive selection
Ensures T cells that do not recognize self do not survive in periphery
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Negative selection
T cells that react to self antigen deleted
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Clonal deletion
T cell that binds repeatedly (e.g. high concentration of self antigen) leads to apoptosis
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Anergy
Recognize self antigen but remains inactive due to lack costimulatory molecules required for its activation
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Active suppression
Kept nonfunctional if self antigen at low levels-these differentiate into regulatory cells-secrete cytokines to prevent other cells from reacting to that antigens
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Ignorance
If self reactive T cell never encounters its antigen--dies from lack of stimulation
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B cell Anergy and Tolerance
Clonal deletion, Anergy, Clonal ignorance
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Type I hypersensitivity-definition
IgE mediated. Immediate. Anaphylactic or atopic.
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Type I hypersensitivity-examples
Urticaria, Allergic rhinitis, asthma, anaphylaxis
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Urticaria
=Hives. Mildest form atopy. Histamine release leads to vasodilation and visible wheal and flare.
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Type II hypersensitivity-definition
Antibody mediated. Activates complement.
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Type II hypersensitivity-examples
Blood transfusions
Erythroblastosis fetalis
Goodpasture syndrome
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Erythroblastosis fetalis
Rh- mother (sensitized) with Rh+ fetus. Mother's antigens attack fetus, can cause brain damage.
Treated with anti-Rh IgG (RhoGAM)
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Goodpasture
anti-GBM, which bind to type IV collagen. Ab complexes in kidney (leading to GN) and lung (leading to pulmonary hemorrhage).
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Type III hypersensitivity-definition
Antigen-antibody complexes form when antigen is abundant. Immune complex deposits in tissues.
Clearance of infections creates antigen-Ab complexes
Some smaller complexes deposit in BV walls-they accumulate in endothelium (vasculitis) and synovium (arthritis)
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Type III hypersensitivity-examples
SLE
Serum sickness
Arthus reaction
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Serum sickness
When serum/Abs, e.g. horse antivenom, administered. +1 week--Abs to foreign proteins, leading to lymphadenopathy, fever, arthralgia, urticarial plaques.
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Arthus reaction
Local swelling at site injection of antigen to which pt immunized. E.g. desensitization allergy shots
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Type IV hypersensitivity-definition
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Cell mediated (delayed).
Initial exposure leads to memory cells. On repeated exposure, effector T cells drawn to site, proliferate, and activate macrophages.
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Type IV hypersensitivity-examples
Tuberculin skin test
| Contact dermatitis
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B cell immunodeficiencies
Transient hypogammaglobulinemia of infancy
Bruton Aggamaglobulinemia
Dysgammaglobulinemia
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T cell immunodeficiencies
Thymic aplasia (DiGeorge)
Chronic mucocutaneous candidiasis
AIDS
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Combined immunodeficiencies
SCID
Wiskott-Aldrich syndrome
Hyper-IgM syndrome
Ataxia Telangiectasia
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Transient hypogammaglobulinemia (of infancy)
Maternal IgG disappearing but infant's B cells not producing sufficient quantities of Abs
81
Bruton agammaglobulinemia
X linked.
Defect in Bruton tyrosine kinase (B cell differentiation, maturation, signaling).
Low amts all Igs.
Recurrent extracellular pyogenic and enterovirus infections.
Tx: IVIG
82
Dysgammaglobulinemia
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Defective B cell class switching.
Most common type is low IgA, thus chronic lung infections (give Abx)
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83
Thymic Aplasia (DiGeorge)
Hypocalcemia, tetany, no T cells
Defective formation 3rd, 4th pharyngeal pouches
Assoc with 22q11 microdeletions
Tx: thymic transplantation
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Chronic mucocutaneous candidiasis
Lack of T cell reactivity (not number) to candida species
85
AIDS
Loss cell mediated (Th) immunity.
| General wasting, constitutional sxs, opportunistic infections
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SCID
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Malfunctioning B and T cells.
Deficiency in adenosine deaminase or purine nucleotide phosphorylase.
X linked version most comm.
Failure to thrive, chronic infections.
Death within 1 year birth if untreated
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87
Wiskott-Aldrich
X linked defect in WASP-defects in actin cytoskeleton.
Affects all hematopoietic cells, esp platelets, T cells.
Pyogenic infections, bleeding diathesis, eczema.
Increased risk AI disorders, lymphoma
Decreased IgM, normal IgA, IgG
Small platelets
88
Ataxia Telangiectasia
AR defect in ATM-insufficient response to DNA damage
Lymphocytes targeted due to high rate proliferation
IgA deficiency and malignancy
Cerebellar ataxia and telangiectasias
Most die mid 20s
89
Phagocyte Deficiencies
Leukocyte Adhesion defficiency
Chronic Granulomatous Disease
Chediak Higashi syndrome
90
Leukocyte adhesion deficiency
AR defect in integrin receptor, which helps phagocytes bind endothelium.
Bacterial infections WITHOUT pus
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Chronic granulomatous disease
Defective NADPH oxidase, involved in ROS killing
Accumulation of immune cells in granulomas.
Infections with catalase positive bacteria or fungal infections.
Test: nitroblue tetrazolium dye.
92
Chediak Higashi sydrome
AR. Failure of vesicle fusion in neutrophils, platelets, melanocytes
Recurrent infections, esp strep and staph.
Increased bleeding, peripheral neuropathy
