Immunity Flashcards
1st line of defense (MIN)
Intact skin
Mucous membranes
normal microbiota
2nd Line of defense (MINCAPFI)
Mass cells and Basophils (inflammatory response) Inflammation Natural killer cells Complement system Anti-microbial substance Phagocytes DEMMN(neutrophils, monocytes; eosinophils, dendritic cells, and macrophages) Fever Interferon
3rd line of defense
Specialized lymphocytes T and B cells Antibodies T lymphocytes Antigen presenting cells B lymphocyts
Prevents microbes from entering airway
Epiglottis
Tears contain ______ which destroy cells walls, gram positive bacteria
Lysosomes.
Traps microbes in respiratory adn GI tract
Mucous
Phagocytes
Cells such as neutrophils, eosinophisl, dendritic cells, and macrophages.
Fever
Intensifies the effects of interferons, inhibits growths of some microbes, speeds up body reactions that aid repair.
***Interferons
Protect uninfected host cells from Viral infection
Interferes with viral replication
Granuloma -
Immune system walls off infectious organisms (fungal or tuberculosis Infections in the lungs). May calcify over time.
is ongoing inflammation. It can be
caused by foreign bodies, persistent pathogens, and autoimmune diseases.
Chronic inflammation.
Short term inflammatory response to an insult to the body
Acute inflammation
*****Repair and healing process
*****IFN-gama (activates macrophages)
TGF-B - (Stimulates fibroblast growth)
Angiogenic factors [VEGF, FGE-2} stimulates endothelial and fibroblast growth
Cellular injury –> Mast cell degranulation
Histamine is released
Cellular injury –> activation of plasma systems. Mast cell degranulation
Histamine is released
*****Mediators of Inflammation
Vasodilation: Prostaglandins, Histamine, Nitric Oxide
Vascular permeablity: Histamine, bradykinin, leukotrienes and , PAF
Pain: Prostaglandins, bradykinin
Systemic effects
Fever : Il-1 , Il-6, TNF alpha, prostaglandins
Acute phase reactants
Leukocytosis
Endogenous pyrogens
Prostaglandin-E2 (PGE2) IL-1 IL-6 TNF-α interferon-γ
Endotoxins of pathogens:
lipopolysaccharide (LPS) component of gram negative bacteria cell wall
Eosinophrils
- Fight PARASYTIC worms infction
2. Regulate and degrade substances.
Neutrophyils (PMN) most ABUNDANT
Phagocytize microorganisms and cellular debris soon after injury FIRST RESPONDERS
Secrete chemical
Natural Killer cells
Eliminate virus infected cells and tumor cells
DESTROY TUMOR/CANCER CELLS
Neutrophyils (PMN) most ABUNDANT
Both (shower and
Phagocytize microorganisms and cellular debris soon after injury FIRST RESPONDERS
Secrete chemical
Natural Killer cells
Eliminate virus infected cells and tumor cells
DESTROY TUMOR/CANCER CELLS
non-PHAGOCYTES, shower with citokines that destroy
Macrophages
Phagocytize microorganinsm and cellular debris
Secrete chemicals that promote tissue healing
Activate adaptive Immunity.
Production
What is arachidonic acid?
Cell membrane PHOSPHOTIDYLCHOLINE gives–>
Phospholipase A2 –> membrane protein Splits into Arachidonic acid and PAF
Arachidonic acid is a 20 carbon polyunsaturate fatty acid precursor to pro-inflammatory molecules
Arachidonic acid gives 2 cyclooxygenase (forms and gives us Prostaglandins 2) and 5-Lipoxygenas (which produces inflammatory leukotrienes)
Production of lipid vasoactive substance by mast cells.
Phospholipase A2 -membrane protein
Arachinoic acid precorse to cyclooxygenase (gives us Prostaglanding 2
Most NSAIDS are
cyclooxygenase
Too much ASA
Bleeding
Complement system (3) main action.
- Chemical signaling. Through NAFTATOXINS (tell white blood cells to kills bacteria , like smelling smoke)
- Starts putting protein molecule on the bacteria, so macrophages destroy. OPSONIZATION- Mark something so macrophages can attack and destroy.
- Punches holes in bacteria wall. (Membrane attack complex)
****________ bind to the cell membrane of the pathogen that activates it, labeling it for ___________
IgG & C3b; phagocytosis (opsonization)
Interferon α -
Produced by Monocytes, has Antiviral action, increases expression of MHC I can be used to treat Hep. B, C
Interferon β -
produced by Fibroblasts, has Antiviral action, increases expression of MHC I can be used to treat MS
Interferon γ -
produced by NK, Tc(CD8), Th(CD4)
Activates Macrophages, increases expression of MHC II, can be used in treatment of cancer
T-cell development in the Thymus (Cortex)
Step 1: Recognize foreign antigen
Step 2: Regonize self antigen
Where T cells are tested
Thymus
Where B cells are tested
Bone marrow
Thymic epithelial cells mechanism of action:
present MHC proteins to the untrained thymocytes
Thymocytes that succesffully bind to the protein MHC continue while those that cannot undergo APOPTOSIS (this is positive selection selecting those that binds)
CD 8 becomes
Cytotoxic T cells.
Which Ig Active against parasites; important mediators of allergic responses
IgE
IgE
- Active against parasites; important mediators of allergic responses
Produced during the primary response to an antigen; are the largest Igs (pentamer)
IgM
- Active against parasites; important mediators of allergic (attach mast cells and basophils) responses
IgE
Produced during the primary response to an antigen; are the largest Igs (pentamer)
IgM
IgM
Produced during the primary response to an antigen; are the largest Igs (pentamer)
Most abundant class of Igs; transported across the placenta
IgG
Has subclasses; one subclass is most abundant in body secretions
IgA
Has subclasses; one subclass is most abundant in body secretions
IgA
IgA
Has subclasses; one subclass is most abundant in body secretions
Serve as surface receptors on developing B lymphocytes
IgD
Serve as surface receptors on developing B lymphocytes
IgD
IgD
Serve as surface receptors on developing B lymphocytes
Dendritic cells (CL -PM)
Capture Antigen from invading pathogen in epithelial tissue
Leave epithelium and migrate to lymphatic vessel
Presents Antigen to immature T cells
Mature T cells multiply and proliferate
Type I hypersensitivity
IgE Medicated hypersensitivity
causes localized and systemic anaphylaxis, seasonal allergies including Hay fever, food allergies such as those to shellfish and peanus , hives and eczema
Type II hypersensitivity
IgG - Mediated Cytotoxic Hypersensitivity.
Red blood cells destroyed by complement and antibody during a transfusion of mismatched blood type or during erythropoiesis fetalis
Type III Hypersensitivity
Immune complex Mediated Hypersensitivity
Most COMMON FORMS of immune complex disease are seen in GLOMERULONEPHRITIS< RA, and SLE
Type IV Hypersensitivity
Cell- Mediated Hypersensitivity
Most common forms are contact dermatitis, Tuberculin reaction, Autoimmune disease such as DM I, MS and RA
**General Four MECHANISMS of Antibodies
Virus neutralization by blocking docking to host cells
Toxin neutrolization
Activate complement-mediated killing
Phagocytosis via opsinisation
*****Class II MHC Distribution
Presents_____
Reacts with _______
B cells, APCs, and some epithelial cells
Exogenous antigens derived from extracellular organisms
CD4 on Th cells
****Class I MHC Distribution –>
Presents_____
Reacts with _______
All nucleated cells and platelets
Endogenous antigens (8-10 amino acids)derived from INTRACELLULAR PROTEINS
CD-8 on Tc Cells
ADCC
Antibody dependent CYtotoxic cell
Does not use CD8 or MHC
Binding to antiboeis
Has receptors for those antibodies.
Epitomes
Specific regions for binding for antigen.
Stages of B cell development in bone marrow.
Stages Stem cell Pro B cell (early, late) Pre-B cells Immature B cell Naive B cell Mature B cell
1st step of complement system
IgE to bindg
Dendritic Cells short version
Capture antigen from invading pathogen in epithelia tissue
Types of APCs
IN skin
Antigen processing and presentation
Reaction when presented to pathogen
Autoimmune dysfunction.
How does Superantigen cause TSS? Bind to MHC class II antigen
Kills all viruses (does not specifically target any particular cell)
STAPH AUREUS EXAMPLE: Toxic Shock syndrome.
The superantigen binds to all T-cells not specific one.–> RELEASE OF EXCESSIVE IL-2
Toxic Shock syndrome can cause
Rash
Desquamation of hands
2 types of adaptive immunity
Naturally acquired
Artificially Acquired.
Mucosal immune Response
MALT such as Peyer’s patches (tonsils) of the small intestine generate ______immunity. Microfold cells (M cells) transport ________
IgA immunity.
antigen inside the body. Dendritic cells then take the antigen to the regional lymph nodes, where an immune response is mounted.
Acute Inflammatory Response system
Cellular injury or pathogenic invasion leads
to:
mast cell degranulation
activation of plasma systems
Release of cellular produces
Complement clotting kinin leads to
Vasodilation Vascular permeability Cellular infiltration Thrombosis stimulation of nerve endings
Mediators of inflammation: What limit inflammation
IL-10 (inhibits cytokine production)
TGF-B (inhibits macrophage proliferation)
ECF-A (Attracts eosinophils)
Histaminage, arylsulfatase (destroy histamine and leukotrines)
Mediators of inflammation: Vascular Permeability
Histamine
Bradykinin
Leukotrienes
PAF
Intact skin forms a physical barrier to entrance of microbes
Epidermis of the skin
Inhibit entrance of many microbes, but not as effective as intact skin
Mucous membranes.
Traps microbes in respiratory and GI tract
Mucous
Provide tears that wash away microbes: tears contain lysozyme which destroy cells especially GRAm POSITIVE BACTERIA
Lacrimal apparatus.
Dilutes and washes microbes from mouth
Saliva
Filters and traps microbes and dust in nose
Hairs
Together with mucous form a ciliary escalator which traps and remove microbes from upper respiratory tract
Cillia
Prevents microbe from entering ear
Earwax
Washes microbes from urethra to prevent colonization
Urine
Move microbes out of body
Vaginal secretions
Expel microbes out of body
Peristalsis
Defecation
Vomiting
Diarrhea
Component of First line defense: Chemical factors
SUP VEGS
Sebum Urine Perspiration Vaginal secretion Earwax Gastric juice Saliva
Both chemical and physical Factors of 1st line defense
Saliva
Urine
Vaginal secretions
Earwax
Components of 2nd line of defense
Defensive cells
Inflammation
Fever
Antimicrobial Substances
Components of 2nd line of defense : Defensive cells are
Phagocytes and
Natural killer cells
Components of 2nd line of defense : Confine and destroys microbes initiate tissue repair
Inflammation
Components of 2nd line of defense : Intensify the effects of interferons, inhibits growth of some microbes and SPEED UP THE BODY REACTION that aid repair
Fever
Components of 2nd line of defense : Kill infected target cells
Kills infected target cells by releasing granules that contain PERFORIN and GRANZYMES –> PHAGOCYTES THEN KILL THE INFECTED MICROBES.
Components of 2nd line of defense : Phagocytosis such a neutrophyills, eosinophils, dendritic cells and macrophages
Phagocytes
Phagocytes are
neutrophils
Eosinophils
Dendritic cells
macrophages
Antimicrobial substance : Complement system
Causes cytosis of microbes, promotes phagocytosis, and contributes to inflammation
Interferons function?
Protect FROM VIRAL INFECTION.
Inhibit growth of certain bacteria by reducing iron
Iron binding proteins.
Describe arachadonic acid. Explain its role in the inflammatory response?
20- Carbon polyunsaturated fatty acid precursor to pro-inflammatory molecules (Cyclooxygenase and 5-Lipooxygenase)
Precursor of Arachidonic acid
Phospholipase A2
T Cell development in the THYMUS (MEDULLA)
The surviving thymocytes move to the thymic medulla where they encounter antigen-presenting cells (APCs) . These APCs present self-antigents from other body ceslls. Thymocytes that bind with the self-antigens undergo apoptosis, as this indicates that they will attack body cells. This is called NEGATIVE SELECTION (selection for cells that don’t bind)
T-cell development in the thymus MEDULLA is the one with the _________ for cells that _____ bind
Negative selection, don’t
Effects of Histamine on Target cells : H1
Target cells (SENM) Smooth muscle cell; endothelial cell; Neutrophil ; Mast cell
Effect of histamine:( Smooth muscle cell) Contraction –> Bronchoconstriction
Effect of histamine on Endothelial Cells:
Contraction (Retraction at endothelial junction)–> Edema and vasodilation
Effects of histamine on Neutrophils:
Increased chemotaxis –> Neutrophil migration
Effects of histamine on Mast cell
Prostaglandin synthesis –> Enhanced Inflammation.
Effects of Histamine on Target cells : H2
Target Cell:
Parietal cell of stomach mucosa
Effect of histamine –> secretion of gastric acid
LENM Lymphocyte : Decreased activity Eosinophils: decreased activity Neutrophil: Decreased chemotaxis Mast cell: Decreased granulation.
Explain mast cell degranulation
Degranulation is a cellular process that releases antimicrobial cytotoxic or other molecules from secretory vesicles called granules found inside some cells. It is used by several different cells involved in the immune system, including granulocytes (neutrophils, basophils, and eosinophils) and mast cells.
Inflammatory Phases 2 fates
Cellular injury –> Acute inflammatory –> healing
Cellular injury –> Acute inflammatory –> Chronic inflammatory –> Glanuloma formation –> Healing
Actions of PGD2 (VIBE)
Vasodilation
Increased capillary permeability
Bronchoconstriction (smooth muscle contraction)
Enhanced inflammation
Actions of PAF (VEBEF VI)
Vasoconstriction Enhanced Inflammation Bronchoconstriction Eosinophils chemotaxis Platelet activation (VI) at low PAF
Actions at H1 receptor
GTP converted to cGMP–> increasing level (cell activation)
Actions at H2 receptor
ATP converted to cAMP –> increasing level –>Cell INACTIVATION
Degranulation immediate response
1. Histamine –> vascular effects
Vasodilation–> Increased permeability –> Exudation
Degranulation immediate response
2.Neutrophil chemotactic factor
Neutrophils attracted to site –> Phagocytosis
Degranulation immediate response
3. Eosinophils chemotactic factor
Eosinophils attached to site –>Phagocytosis
Synthesis long term response
Leukotrienes and Prostalginding E- series
Vascular effects–> Dilation and increased permeability–> EXUDATION
T cells and B cells can be activated only by
exposure to a specific antigen at a specific site in a plasma membrane.
When an antigen is bound to a Class II MHC protein, it can activate a ________ cell.
B helper Cells
Class II MHC molecules are found on which of the following?
Lymphocytes and APCs
When an antigen is bound to a Class I MHC molecule, it can stimulate a ________ cell.
CYTOTOXIC T cells
Cell mediated immune response in order: Several cycles of mitosis occur.
- Antigen is engulfed and presented by a macrophage.
- Cytotoxic T cells migrate to focus of infection.
- T cells with specific receptors recognize the antigen.
- T cells differentiate into cytotoxic T cells or T memory cells.
- Cytotoxic T cells release perforin and/or lymphotoxin.
B) 2, 4, 1, 5, 3, 6
Antigen is engulfed and presented by a macrophage
T cells with specific receptors recognize the antigen
Several cycles of mitosis occur.
T cells differentiate into cytotoxic T cells or T memory cells.
Cytotoxic T cells migrate to focus of infection.
Cytotoxic T cells release perforin and/or lymphotoxin
Immunity that results from antibodies that pass through the placenta from mother to fetus is called ________ immunity.
Naturally acquired passive
The first line of CELLULAR DEFENSE Against PATHOGENS
Phagocytes
Most of the lymph returns to the venous circulation by way of the
THORACIC DUCT
Lymphatic tissue is found in the greatest quantity in
A) the adult spleen.