host immune response Flashcards
N formyl methionyl-
mediate antimicrobial responses
Mannose receptors
initiate phagocytosis of microbes
Scavenger receptors
phagocytosis of cell debris
Cytokines-
proteins made by cells that mediate inflammation
Principal mediators of communication between cells of the immune response
cytokines
Chemokines-
cytokines that tell WBC to go from the blood to tissues
How Phagocytes degrade microbes:
Microbe binds to phagocyte
Phagocyte zips around microbe
Microbe ingested in phagosome
Phagolysosome- ROS and NO kill microbe in phagolysosome
NK cells-
nonspecific, kill virus and tumor cells, first responder
Neutrophils/PMN-
phagocytose organisms, cause tissue damage in inflammation, first responder
2 first responders
NK cells and PMN
Eosinophils-
parasites, allergic rxns in skin and airway
Macrophages-
Phagocytose and kill intracellular microbes
Kill infected or changed self cells
Help in tissue repair/wound healing
APC
Dendritic cells
process antigen and present it to T cells to initiate the adaptive immune response
links adaptive and innate immune system
dendritic cell
also make cytokines and phagocytose cells, but MAIN job is antigen presentation
dendritic cell
Innate immune response common to all pathogens (know):
Phagocytosis and killing of microbes
Antigen presentation
Cytokine production
TLR 2 and 4
extracellular/on cell surface; on all cells
TLR 9
intracellular
Adjiment-
enhance immune response by attaching to TLR and creating pathways in a vaccine
Dendritic cells are immature in periphery and mature once they get to the lymph node (know)
Dendritic cells become mature
Pick up an Ag which activates a TLR
Cytokines are made in the LN based on what TLR was activated
Chemokines are secreted into periphery to warn other cells
APC:
DC- mainly
Macrophages
B cells
endogenous Ag
Ag made in the body during normal metabolism or viral infection
NK cells important
Presented to APC by CD8+T cells
MHC class I
exogenous Ag
Ag enters the body from the environment Can be inhaled, ingested, or injected B cells and Ab are important Ag presented by APC to CD4 + T cells MHC class II
CD8+T cells are MHC I and recognize
cytosolic proteins such as viruses
CD4+T cells are MHC II and recognize
extracellular and intravesicular pathogens such as bacteria
Humoral response:
Mature B lymphocytes make antibodies
Naive B cells do NOT make antibody
what do Antibodies do
Neutralize microbes
Enhance phagocytosis via opsonization
have a membrane bound IgM and Ig cant be secreted
resting or naive b cells
Plasma cell
secrete Ab; either IgM, IgA, IgE, IgD, IgG
wait for 2nd exposure to the Ag and secrete Ig when it encounters it
Memory cell
In mucosal areas such as the gut, resp tract, urogenital tract
In tears, saliva, and breast milk
IgA
Majority of Ab
Crosses the placenta
Shows memory/immunity to an infection
IgG
1st secreted during an active infection
Eliminated early pathogens of B cell mediated immunity before there is enough IgG
Expressed on surface of B cells
IgM
Antigen receptor on naive B cells
Activated basophils and mast cells to make antimicrobial factors
IgD
Binds to allergens and triggers histamine to be released from mast cells and basophils
Similar to eosinophil
Protects against parasites
IgE
IgG types?
4
Epitope-
fragment that binds MHC molecule so TCR can recognize it
Immunodominant epitope-
epitope where most of the responding T cells are specific, usually the ones that have the highest affinity for binding to MHC
Th0-
naive; havent seen Ag
Th1
Promote cell mediated immunity
Mediates delayed hypersensitivity rxns (type 4)
T cells mediated, autoimmunity, graft rejections
Make cytokine INF gamma
Activates macrophages
Th2
Promotes humoral immunity Allergy, Ab mediated autoimmune disease, tolerance Makes cytokine IL4 Activates B cells to make Ab Limites inflammatory response
Th17
Promotes inflammation in autoimmune responses
Secretes IL17
Combats infections and mediates autoimmunity
Treg
Suppresses immunity
Autoimmune regulation
Contact dependent
Secretes cytokines IL10 and TGF B
FAS and FAS ligand causes
aopotosis
Granzymes-
enzymes enter holes and causes apoptosis
type 1 hypersensitivity
Classic allergy
IgE mediated
Immune system responds to harmless antigen from environment
Antigen binds to IgE antibodies on mast cell or basophil. Mast cell or basophil then releases histamine
type 1 hypersensitivity examples
Allergic rhinitis, asthma, food allergy, drug rx, anaphylactic shock
type 2 hypersensitivity
Ab and complement mediated
IgM or IgG antibodies bind to antigen covalently bounded on the cell membrane which activate the complement cascade. Then MAC is formed and the cell is destroyed
type 2 hypersensitivity examples
Hemolytic anemia, ABO transfusions, autoimmune hyperthyroidism
Type 3 hypersensitivity
Immune complex mediated
Complexes deposited in tissues or vascular endothelium
type 3 hypersensitivity examples
Authrus, serum sickness, GN, RA, SLE
type 4 hypersensitivity
Transmitted by immunologically sensitized T cells (CD4 or 8), NOT serum
Starts hours after exposure and lasts days
Mediated by CD4 T cells
type 4 hypersensitivity examples
Contact hypersensitivity
Tuberculin hypersensitivity
Effects of complement:
cytolysis, opsonization, chemotaxis, anaphylatoxin, enhancement of Ab production
cytolysis
C5b, 6, 7, 8,9 insert into bacterial, RBC, or tumor cell membrane and lyse cell
Opsonization
C3b on phagocytes
Chemotaxis
C5a and the C5,6,7 complex attract neutrophils
Anaphylatoxin
C3a, C4a, and C5a degranulate mast cells
Enhancement of Ab production
C3b binds to activated B cells which makes Ab
Deficient in C3b?
youll get a lot of pyogenic infections
Complement-
plasma proteins and cell membrane receptors that mediate host defenses and inflammation
End result of complement activation:
MAC and target cell death
complement pathways
Classical pathway- antigen antibody complexes
Alternative- interact with bacteria
