Immunology Flashcards
Innate Immunity
Non-specific
First line of defense
No memory
Specific Immunity
Recognition of pathogen
Faster response everytime
Memore involved
Lymphoid Organs
Primary: stem cells divide = immune cells develop
Secondary: where the response occurs
Primary Lymphoid Organs
Bone Marrow: RBCs are produced, B-cells and Immature T-cells
Thymus: T-cells, dendritic cells, macrophages
Secondary Lymphoid Organs
Lymph nodes: filter microbes, macrophages present
Spleen: removed microbes and old erythrocytes
Lymphoid nodules
Immune Cells Origin
Derived from pluripotent hematopoietic stem cells
Lymphoid stem cell
- Lymphocytes: T cells, B cells, Natural Killer cells
Myeloid stem cell
- Macrophages, dendritic cells
Cytokines
Secreted by immune cells to regulated host cell division and function (innate and adaptive)
First line of defense
Skin: water resistant
Tight junctions, mucus, hair, cilia, secretions
Secondary line of defense
Humoral Factors
Cellular Factors
Inflammation
Humoral Substances
Discourages microbial growth/ spread
1. Interferons
2. Complements
3. Iron-Binding Proteins
Complement Activation
Recruitment of inflammatory cells
Opsonization (prepare for eating) of pathogens
Killing of pathogens
Phagocyte binds to pathogen and absorbs it
Inflammation
Mast cells circulate and look for antigens = signals with histamine
1. Vasodilation (widen blood vessel = increased blood flow, increased permeability to capillaries)
2. Emigration of phagocytes
3. Tissue Repair
Interferons
Detects antigen and notifies the body = triggers Natural Killer cells (First responders)
Cellular Factors
Natural Killer Cells
Phagocytes
Natural Killer Cells
Detects when our own cells are infected (have gone rogue)
Lymphocyte that attacks and kills target cells after binding to them
Not antigen specific
MHC Class 1
MHC Class 1
Expressed on all normal nucleated body cells = NK cell recognizes it and does not kill that cell
Altered MHC Class 1 proteins cannot stimulate negative response = NK cell releases agents that kill the cell
Phagocytes (macrophages, neutrophils, dendritic cells)
Kill old RBCs in spleen
Non-specifically engulf microbial invaders
Phagocytosis/ Intracellular Destruction of Microbe
- Endocytosis
- Phagosome created in phagocyte (vesicle with microbe)
- Lysosome merges with phagosome (low pH, w/ corrosive enzymes digest the microbe)
- Phagolysosome forms = digestion
- Release of end product
How do Phagocytes Recognize Microbes
Detects PAMPs on surface of microbes
Immune system receptors are PRRs on the surface of macrophages
Activation of Phagocytes
- Margination: adhesion to capillary wall
- Diapedesis: phagocytes moves across wall
- Chemotaxis: chemoattractants bring phagocytes to damaged area
- Neutrophils die in the process of killing microbe- Pus is produced (dead bacteria and neutrophils)
Dendritic cells
Eat bacteria and bring information to create antigens (from surface of microbe)
Link between innate and adaptive
Antigen
Triggers antibody production
Has specific epitopes
Epitope
Part of antigen that is recognized by immune cell
Adaptive Immunity
Via antigen presentation by phagocytes
Macrophage and dendritic cells bring antigen to lymph node to activate specific response
Humoral-Antibody-Mediated Immunity
Involves B cells
- transform into plasma cells
- synthesize and secrete antibodies
- memory B cells
Cell-Mediated Immunity
Involves cytotoxic T cells
- kills infected body cells, cancer cells and foreign cells
Major Histocompatibility Complex (MHCs)
How NK cells know which cells to kill
- MHC Class 1: present on all normal nucleated body cells
- MHC Class 2: expressed on antigen-presenting cells (macrophages, dendritic cells, B cells)
Antigen Presenting Cell Formation
- Phagocytosis of exogenous antigen
- Digestion of antigen into peptide fragments
- Synthesis of MHC-II molecules
- Packaging of MHC-II molecule into vesicle
- Vesicles with antigen peptide fragments and MHC-II fuse
- Antigen peptide fragment binds to MHC-II molecule
- Vesicle exocytosis and antigen MHC-II complexes are inserted into plasma membrane (identification)
Checkpoint inhibition
Shut off control of T cell activation
CTLA4 binds to antigen presenting cell and deactivates T cell
Antibody Structure
Immunoglobin
2 heavy chains
2 light chains
Variable region: antigen binding site
Constant region: same in all antibodies (Fc)
Antibody Classes
Determined by Fc
Types: IgG, IgA, IgM, IgD, IgE
Active Immunity
Person’s own immune system responds to microbe
- Long lasting protection due to memory cells
Natural Active Immunity
When someone is exposed to microbe by chance
ex: flu
Artificial Active Immunity
When someone is purposefully exposed to microbe
ex: flu shot
Vaccine
Small quantities of living or dead pathogens cells derived from antigen’s source
Exposure to antigenic substance results in an active immune response that induces formation of memory cells, so that natural exposition doesn’t trigger a large immune response
Passive Immunity
Person receives antibodies from another person/ animal
- temporary protection = no memory cells
Natural Passive Immunity
IgG from mother to fetus across placenta or IgA in breast milk
Artificial Passive Immunity
Receive serum containing antibodies from person/ animal that was vaccinated
Antibody Function
- Neutralizing antigen
- Agglutinating antigen
- Precipitating antigen
- Activating complement
- Opsonization (prepare to eat)
Second exposition
Rate of antibody production after initial exposure will be higher because system is familiar with antigen
Self antigens
MHC makes sure immune system doesn’t attack its own cells
Important for tissue/ organ transplant rejection
Somatic Hypermutation
During development of cells, DNA is recombined so that each cell is only capable of one specific variable region
IgG and IgA
IgG is higher in secondary response - it moves throughout the body
IgA is only found in mucosal tissues
Development of T Cell Tolerance
T cells that can’t recognize MHC-I molecules are destroyed
T cells that destroy cells with MHC-I molecules are destroyed
T cells
Require activation - when binds to foreign antigen
- Helper T cell
- Cytotoxic T cell
Endogenous Antigen
Produced by your own body
Infected Body cells will have altered MHC-I
Exogenous Antigen
From outside source
Antigen presenting cell is recognized and MHC-II is placed in it’s membrane
Cell-Mediated Killing of Virus Cell (or infected cells)
- pathogen presents its MHC-II = activation of helper T cell
- helper T cell releases cytokines = activate cytotoxic T cell
- Tc binds to infected cell on MHC-II and kills it by releasing perforins and granzymes
(self infected cells would be the same but with altered MHC-I)
Factors Changing Resistance to Infections
Protein-calorie malnutrition
Preexisting disease
Stress
No exercise
Sleep deprivation
Immunodeficiency Diseases
SCID: absence of B and T cells, sometimes lack NK cells
AIDS: infects and kills helper T cells (can’t trigger adaptive immune response)
Tissue Graft/ Organ Rejection
Has to do with difference in MHC-I proteins on recipient and donors macrophages in tissue
Can be recognized as foreign by Helper T cells
Cyclosporine
Immunosuppressant drug that blocks the production of cytokines secreted by T(H) –> eliminates proliferation of Tc and T(H) cells
Problem: decreases immune system
Transfusion Rxns
Antibody compatibility for different blood types
A: antigen A; antibody anti-B
B: antigen B; antibody anti-A
AB: antigen B and B; neither anti-A nor anti-B
O: neither A or B; Both antibody anti-A and anti-B
Allergic Rxn
When a person’s immune response is overly reactive to a substance that most tolerate well
Mast cells are involved - inflammation (histamines)
Anaphylaxis
Localized at site of injection or
Large amounts of chemicals spread out and cause inflammation in circulatory system = constriction
Autoimmune Disease
Body triggers response against own antigens
Mediated by autoantibodies + self reactive T cells (can’t identify MHC-I molecules)
ex: Type I Diabetes, Rheumatoid Arthritis, Multiple Sclerosis
