Immunology Flashcards
Basophils
Granulocyte Least common Mature in bone marrow Circulate in blood stream Release histamine and heparin (allergic and helminth response)
Eosinophils
Derived from bone marrow, 1-6% of WBCs Bloodstream and organs (GI &respiratory) Release H2O2 and oxygen radicals to kill viruses/parasites Release leukotrienes Active in allergic reactions, asthma Stimulate T-lymphocytes Antigen presenting Cell weakly phagocytic
Leukotriene
lipid signaling molecule that causes airway muscle contraction
Neutrophils
Most abundant granulocyte Circulates bloodstream "first responder" (bacteria and fungi) Releases cytokines Strongly phagocytic Neutrophil extracellular traps
Cytokines
Cell to cell communication proteins that control development, differentiation and movement to specific part of body
Interleukins, TNF, Chemokines, Interferons
Interleukin
13 cytokines that are regulators of immune response, inflammatory response and hematopoiesis
ILs 1&6-fever
IL 6-“acute phase” response
Tumor Necrosis Factor (TNF)
activates neutrophils, mediates septic shock, causes tumor necrosis
Chemokines
cytokine released by infected/injured cells-imitate immune response (signal neutrophils and macrophages) and warn neighboring cells of threat
Interferons
Block virus replication
Alpha, beta, gamma
Gamma is strongest-produced by Tcells, activates macro/NK/neutro
Mast Cells
Release histamine and heparin
Naive in bone marrow, mature in tissues
Degranulate (burst) if injured, encounter antigen/allergen, exposed to complement protein
Causes anaphylaxis
Monocyte
“Agranular”
Give rise to dendritic and macrophages
Develop in bone marrow>spleen and tissues
Differentiate in tissues
3 functions: phagocytosis, APC, cytokine production
Dendritic cell
Strongest of APCs Activate T-helper cells Capture antigen migrate to lymph node and present to T and B cells Langerhans cells
Macrophage
Large phagocyte release TNF and ILs Act as APCs to helper T cells Under skin, lungs, GI, respiratory 3 stages: resting-cleaners, Primed-active engulfing/APC, Hyperactivated-rapidly destroying pathogens
Kupffer Cell
Specialized macrophage within liver
destroy bacteria and old RBC
Chronic activation leads to overproduction of inflammatory cytokines
Causes liver damage/cancer
May become host for TB, Leishmania, Cikinguya
Natural Killer Cells
Cytotoxic lymphocytes against viruses and cancer cells
granules of destructive enzymes
Mature in bone marrow, lymph nodes, spleen, tonsils and thymus
enhanced by cytokines
Release performs and protease that lyse cell or trigger apoptosis
Can trigger apoptosis by surface contact
in bloodstream, liver and spleen
“kill or don’t kill”
Can kill during resting phase
Major Histocompatibility Complex (MHC) Proteins
AKA Human leukocyte antigen (HLA)
surface molecules that help determine if protein is “self” or “not self”
Bind antigen to cell surface and display for T-cell recognition
3 subgroups (I, II, III)
Determines organ donation compatibility
malfunction causes autoimmune diseases
T and B cell activation
Acute Phase Proteins
Produced by liver in response to release of IL-1, IL-6 and TNF
C-reactive protein, Mannose-binding lectin, lipopolysaccharide-binding protein
Mark pathogens/injured cells for destruction-activates complement
Complement system
Enhances ability of phagocytic cells to destroy pathogens
3 possible activation pathways: Classical (requires trigger), Alternative (continuously activated at low level), &Lectin pathway (requires very specific type of trigger)
ACTIVATED BY ANTIGENS
proteins made by liver
C3 most abundant in humans
Opsonization
enhancing phagocytosis of antigens by “marking” them for destruction
Chemotaxis
Attracting and activating macrophages and neutrophils; inducing mast cells and basophils to degranulate
Lysis
Rupturing pathogen cell-membranes by forming the Membrane Attack Complex (MAC)
Complement Fixation
Antigen combines with an antibody and it’s complement, causing the complement factor to become inactive or “fixed”
Membrane Attack Complex
C5b forms complex with C6, C7, C8 and C9 to form MAC
causes lysis of cell by disrupting osmotic balance (bringing water into cell), which causes the cell to swell and burst
Innate Immunity
Immediate response
Non-specific response (always the same)
Response doesn’t increase with repeat exposure
Adaptive Immunity
Antibodies recognize only ONE antigen, binds to specific site on invader
Directly block binding of invader cells, Inactivate viruses/neutralize toxins, Mark pathogen for destruction by phagocytes
Requires days to develop
Responce enhanced by repeated exposure (develops memory for quicker/more intense response)
Antibody
2 light chains, 2 heavy chains, antigen binding sites, FAB region, Fc region
IgM, IgG, IgE
IgM
Primary immune response
Half life of ~10 days
usually in intravascular space
increased levels=RECENT exposure to antigen
IgG
4 subclasses
Found in Blood, lymph, CSF, peritoneal fluid
Evenly distributed in intra/extravascular space
Only class that crosses placenta-Rh antigen, but gives baby moms immunity
Helps NK find their target (opsonization), immobilize bacteria by binding to cilia/flagella, activates complement, neutralizes toxins and some viruses by binding
Late in primary response
IgA
Primarily in external secretions (including breast milk)
Protects infant, prevents viruses from entering cell, prevent pathogens from attaching to/penetratin epithelial surfaces
IgE
Low amounts in serum
2 day half life
Binds to mast cells and basophils
Triggers degranulation, releasing histamin/leukotrienes/heparin from granulocytes
Increased in atopic people & in presence of parasites
IgD
Present on surface of naive B cells
low amounts in serum
unknown function
Primary Lymphoid organs
Thymus and Bone Marrow
where immature lymphocytes go to mature/proliferate
Secondary Lymphoid Organs
Spleen, lymph nodes, tonsils/adenoids, appendix
Where antigens presented to mature B & T lymphocytes to imitate adaptive immune response
B-Cell
Elliminates extracellular pathogens
Antigen-presenting cell w/ MHC
Produces antibodies (immunoglobulins, Ig) to neutralize pathogen
Has membrane-bound antibodies, recognizes antigen by B-cell receptor coupled with T-helper, prompts B-cell to divide into effector cells which produce antibodies
Produce memory B cells
T-Cell
Destroy intracellular pathogens (viruses/intracellular bacteria)
Directly kill infected cells